Zinc Overview |
Zinc is an essential trace mineral necessary for the proper function
of about 300 different enzymes. Therefore, zinc plays a role in virtually
all biochemical pathways and physiological processes in the body. Thirty
percent of the body’s zinc is stored in the bones and 60% in muscles.
The other 10% is found in virtually all body tissues. Zinc is important
for wound healing; immune system support; to reduce length and severity
of colds (in lozenge form); to support a healthy prostate gland (prevents
benign prostatic hyperplasia – BPH); and to increase fertility (sperm
production). It also assists digestion, energy production, growth, cellular
repair, collagen synthesis, bone strength, cognitive function, and carbohydrate
metabolism (glucose utilization and insulin production). Even mild zinc
deficiency has been associated with depressed immunity, decreased sperm
count and impaired memory.
Dietary Sources: The richest dietary sources of zinc
are seafood (especially oysters), meat, fish, eggs, and poultry.
Dosage: The RDA for zinc is 15mg per day. As therapy
for colds, however, higher levels are required – with levels in
the range of 13-23mg (in lozenge form) taken every 2 hours for no more
than 2 weeks effective for reducing duration and severity of cold symptoms.
Side Effects: The short-term use of zinc at therapeutic
doses for cold relief (see below) is assumed to safe and chronic supplementation
with zinc at levels 2-3 times the current RDA should not be expected to
pose any significant adverse side effects. However, high doses of zinc
are not recommended for periods of more than two weeks due to interference
with copper absorption. High doses of zinc (gram levels) can cause nausea,
diarrhea, and vomiting.
(Source: www.supplementwatch.com)
Research Overview
Deficiency in zinc has been shown to contribute to:
1. Hypogonadism
2. Testicular dysfunction
3. Atrophy of testes
4. Decreased sperm motility
5. Decreased sperm count
6. Sperm cell death
7. Unwanted weight loss
8. Impaired taste functioning
9. Poor appetite
10. Dermatitis
11. Acrodermatitis enteropathica
12. Alopecia
13. Night blindness
14. Delayed wound healing
15. Diarrhea
16. Delays in cognitive development
17. Impaired memory
18. Impaired capacity to learn
19. Decreased activity levels
20. Decreased attention performance
21. Increased susceptibility to infectious diseases
22. Juvenile and adolescent growth delays
23. Delayed puberty
24. Stunted brain and body growth
25. Stunted organ growth
26. Tinnitus
27. Dwarfism
28. Bone mineral loss and osteoporosis
29. Impaired immune functioning
30. Impaired platelet aggregation
31. Reduction in natural killer cell activity
32. Impaired female reproductive processes
33. Decreased growth hormone production
34. Higher risk of esophageal cancer
35. Adverse lymphocyte production and maturity
36. Insulin resistance
37. Weakened thyroid hormone metabolism
38. Atrophy of thyroid gland
39. Decreased basal metabolic rates
40. Potentially increase neuronal dysfunction in Alzheimer’s and
Down’s Syndrome
Zinc supplementation was found to:
1. Enhance efficacy of interferon therapy in Hepatitis C
2. Improve bacterial prostatitis
3. Prevent hepatic encephalopathy
4. Prevent alcohol induced liver damage
5. Prevent esophageal cancer
6. Improve night vision
7. Work synergistically with vitamin A
8. Improve halitosis
9. Reduce plaque buildup in teeth
10. Reduce duration and severity of the common cold
11. Reduce incidence of pneumonia when taken with vitamin A
12. Reduce severity and duration of chronic diarrhea
13. Prevents damage from mercury exposure
14. Reduce anxiety and depression
15. Increase weight gain in anorexia nervosa
16. Increase weight gain and growth in children with sickle cell disease
17. Improve thyroid function
18. Enhance efficacy of thyroid hormone supplementation
19. Improve immune function
20. Decrease oxidative stress
21. Enhance efficacy of tuberculosis treatment when combined with vitamin
A
22. Decrease blood glucose levels
23. Inhibit the development of Type I diabetes
24. Improve libido
25. Increase sperm count
26. Increase frequency of sexual intercourse
27. Treat delayed adolescent sexual development
28. Treat hypogonadism
29. Treat recurrent aphthous stomatitis
30. Improve tinnitus
31. Treat Alzheimer’s disease
32. Act as a topical antioxidant
33. Improve neurological recover in brain injury
34. Protect cells from drug toxicity (AZT)
35. Reduce incidence of infection in AIDS
36. Treat dandruff
37. Potentially reduce incidence and severity of fetal alcohol syndrome
38. Improve liver function in alcoholic cirrhosis
39. Reduce inflammation and promotes stomach ulcer healing
40. Improve wound healing
41. Reduce bone loss in osteoporosis
Zinc
Abstracts (91)
Zinc
Citations (1000)
|
Zinc: 91 Research
Abstracts |
Acne
1. Endotoxin-induced changes in copper and zinc metabolism in the Syrian
hamster.
Etzel KR, Swerdel MR, Swerdel JN, Cousins RJ
J Nutr 1982 Dec;112(12):2363-73
The temporal response of zinc and copper metabolism to endotoxin administration
was examined in Syrian hamsters over a 144-hour period. Serum copper was
significantly elevated at 12, 24 and 72 hours after endotoxin, whereas
serum zinc was reduced 4-48 hours after treatment. A brief elevation (8
hours) in liver copper concentration and a sustained (72 hours) increase
in liver zinc concentration were also observed. The amount of zinc associated
with liver metallothionein (MT) progressively increased with time, to
a plateau by 24 hours and persisted at the elevated level until 72 hours
after endotoxin treatment. In vitro translation of poly (A)+ RNA from
liver polyribosomes showed that following endotoxin treatment MTmRNA activity
was maximally elevated 6 hours after endotoxin administration and remained
elevated 24 and 48 hours thereafter. Slab gel electrophoresis of serum
proteins indicated changes in a stainable protein comigrating with purified
ceruloplasmin after endotoxin administration. Pooled gingival tissue from
endotoxin-treated hamsters demonstrated a consistently elevated copper
content 12-144 hours after treatment. Endotoxin isolated from Bacteroides
melaninogenicus was more effective in elevating gingival and serum copper
and gingival zinc than Escherichia coli endotoxin. It was concluded that
endotoxin administration elicits responses that result in enhanced metaollthionein
mRNA activity. In addition, Cu and Zn concentrations in serum, liver and
gingival tissue are influenced by different endotoxins to different degrees.
2. [Current aspects about the role of zinc in nutrition]. [Article in
French]
Favier A Groupe de recherche sur les pathologies oxydatives, Universite
de Grenoble, La Tronche.
Rev Prat 1993 Jan 15;43(2):146-51
The role played by zinc in biology is now better known, and numerous
biochemical mechanisms, such as immunity or actions on several hormones
and more than 200 enzymes, have proved to be zinc-dependent. Thus, many
functions are disturbed when this trace metal is deficient, including,
for example, taste and appetite, cell multiplication, growth, pregnancy,
fertility, defence against bacteria and brain functions. Zinc intake has
been found to be unexcessive and indeed, at the limit of sufficiency in
the French population. Groups at risk, such as neonates, growing children,
pregnant women and elderly people, should have a higher zinc intake provided
by dietary measures or supplementation. Zinc supplementation has been
shown to exert a beneficial effect in randomized studies concerning children's
growth, acne, old people's immunity or low female fertility. Such supplementation
must be balanced and given in moderate doses since zinc interacts with
other foodstuffs, and an excess of zinc can be as bad as its deficiency
in our nutrition.
3. Effects of oral zinc and vitamin A in acne.
Michaelsson G, Juhlin L, Vahlquist A
Arch Dermatol 1977 Jan;113(1):31-6
The effects of oral zinc sulfate (corresponding to 135 mg of zinc daily)
alone and in combination with vitamin A (300,000 international units)
daily on acne lesions have been compared with those of vitamin A alone
and of a placebo. The number of comedones, papules, pustules, and infiltrates
were counted at each visit. After four weeks, there was a significant
decrease in the number of papules, pustules, and infiltrates in the zinc-treated
groups. The effect of zinc plus vitamin A was not better than zinc alone.
After 12 weeks of treatment, the mean acne score had decreased from 100%
to 15%. The mechanism for the effect of zinc therapy in acne, to our knowledge,
is not presently known.
4. Serum zinc and retinol-binding protein in acne.
Michaelsson G, Vahlquist A, Juhlin L
Br J Dermatol 1977 Mar;96(3):283-6
The serum levels of zinc and retinol-binding protein (RBP) have been
determined in 173 patients with acne and compared with those of a control
group. The RBP is a specific transport protein and its level in plasma
reflects the amount of vitamin A available to the tissues. Patients with
severe acne were found to have lower levels of RBP than either patients
with mild acne or healthy subjects of the same age. In the case of males
with severe acne, the mean serum zinc level was significantly lower than
that of the control group. No such difference was observed for girls.
The observed condition of low levels of zinc and vitamin A in the serum
of patients with severe acne may provide a rationale for the clinically
good effect of oral zinc treatment.
5. A double-blind study of the effect of zinc and oxytetracycline in
acne vulgaris.
Michaelsson G, Juhlin L, Ljunghall K
Br J Dermatol 1977 Nov;97(5):561-6
With a double-blind technique, the effects of oral zinc and tetracyclines
were compared in 37 patients with moderate and severe acne. No difference
in effect between the treatments was seen and no side-effects were noted
in any group. After 12 weeks of treatment, the average decrease in the
acne score was about 70% in both groups.
6. A double-blind controlled evaluation of the sebosuppressive activity
of topical erythromycin-zinc complex.
Pierard-Franchimont C, Goffin V, Visser JN, Jacoby H, Pierard GE Department
of Dermatopathology, University of Liege, Belgium.
Eur J Clin Pharmacol 1995;49(1-2):57-60
In a double-blind randomised study, 14 volunteers applied 4% erythromycin
plus 1.2% zinc (Zineryt lotion) and 4% erythromycin lotions, each on half
of the forehead twice daily for 3 months. The sebum output was evaluated
at 3-week intervals using the photometric and the lipid-sensitive film
methods. Evaluations of casual level (CL) and sebum excretion rate (SER)
were made with a Sebumeter, and total area of lipid spots (TAS) was measured
on Sebutapes. Compared to baseline values, the formulation of the erythromycin-zinc
complex induced significant reductions in SER after 6 and 9 weeks, and
in CL and TAS at 3, 6, 9 and 12 weeks. The mean reduction in TAS was over
20% for four successive 1-h samplings on completion of the study. Significant
reductions in CL, SER and TAS were observed for the erythromycin-zinc
formulation compared to the control lotion at 6 and 9 weeks, and also
at 3 weeks for SER and TAS, and at 12 weeks for CL and TAS. This study
indicates that sebum output is significantly reduced by the erythromycin-zinc
complex. This reduction is theoretically beneficial for the acneic patient.
7. Zinc sulfate in acne vulgaris.
Weimar VM, Puhl SC, Smith WH, tenBroeke JE
Arch Dermatol 1978 Dec;114(12):1776-8
The effects of orally administered zinc sulfate in 52 patients with mild
to moderate acne vulgaris were compared to those of a placebo capsule.
The numbers of comedones, papules, pustules, infiltrates, and cysts were
counted at each visit over a 12-week period. Forty patients completed
the study. Zinc appeared to have a somewhat beneficial effect on pustules
but not on comedones, papules, infiltrates, or cysts. Fourteen patients
(50%) in the zinc group had side effects of nausea, vomiting, or diarrhea.
Six patients (21%) in the zinc group could not tolerate the nausea and
withdrew from the study.
8. Inhibition of erythromycin-resistant propionibacteria on the skin
of acne patients by topical erythromycin with and without zinc.
Bojar RA, Eady EA, Jones CE, Cunliffe WJ, Holland KT Department of Microbiology,
University of Leeds, U.K.
Br J Dermatol 1994 Mar;130(3):329-36
Propionibacteria resistant to high concentrations of erythromycin [minimal
inhibitory concentration (MIC) > or = 0.5 mg/ml] are now commonly
isolated from the skin of antibiotic-treated acne patients. This double-blind
study was carried out to assess the ability of 4% w/v erythromycin with
and without 1.2% w/v zinc acetate to reduce the numbers of erythromycin-resistant
propionibacteria in vivo, and also to monitor the acquisition of resistant
strains de novo during therapy. Under laboratory conditions, erythromycin-resistant
propionibacteria were shown to be as sensitive to zinc acetate as fully
sensitive strains. In vivo, the erythromycin/zinc complex and erythromycin
alone produced highly significant reductions in total propionibacteria
(P < 0.001) and in the number of erythromycin-resistant strains
(P < 0.001 at 8 weeks). After 12 weeks, resistant propionibacteria
were reacquired, or acquired de novo, by three patients treated with erythromycin
alone and four patients treated with the erythromycin/zinc complex. In
contrast, changes in numbers of Micrococcaceae were slight and, after
12 weeks, erythromycin-resistant strains were predominant in both treatment
groups. In vitro MIC determinations suggested that this finding might
be explained by the exceptionally high degree of erythromycin resistance
displayed by some staphylococcal strains (MIC > 4 mg/ml) and by
the relative insensitivity of all staphylococcal strains to zinc acetate.
Erythromycin with and without zinc was clinically effective, and both
preparations produced significant reductions in acne grade, and inflamed
and non-inflamed lesion counts (P < 0.001).
9. Endotoxin-induced changes in copper and zinc metabolism in the Syrian
hamster.
Etzel KR, Swerdel MR, Swerdel JN, Cousins RJ
J Nutr 1982 Dec;112(12):2363-73
The temporal response of zinc and copper metabolism to endotoxin administration
was examined in Syrian hamsters over a 144-hour period. Serum copper was
significantly elevated at 12, 24 and 72 hours after endotoxin, whereas
serum zinc was reduced 4-48 hours after treatment. A brief elevation (8
hours) in liver copper concentration and a sustained (72 hours) increase
in liver zinc concentration were also observed. The amount of zinc associated
with liver metallothionein (MT) progressively increased with time, to
a plateau by 24 hours and persisted at the elevated level until 72 hours
after endotoxin treatment. In vitro translation of poly (A)+ RNA from
liver polyribosomes showed that following endotoxin treatment MTmRNA activity
was maximally elevated 6 hours after endotoxin administration and remained
elevated 24 and 48 hours thereafter. Slab gel electrophoresis of serum
proteins indicated changes in a stainable protein comigrating with purified
ceruloplasmin after endotoxin administration. Pooled gingival tissue from
endotoxin-treated hamsters demonstrated a consistently elevated copper
content 12-144 hours after treatment. Endotoxin isolated from Bacteroides
melaninogenicus was more effective in elevating gingival and serum copper
and gingival zinc than Escherichia coli endotoxin. It was concluded that
endotoxin administration elicits responses that result in enhanced metaollthionein
mRNA activity. In addition, Cu and Zn concentrations in serum, liver and
gingival tissue are influenced by different endotoxins to different degrees.
10. [Current aspects about the role of zinc in nutrition]. [Article in
French]
Favier A Groupe de recherche sur les pathologies oxydatives, Universite
de Grenoble, La Tronche.
Rev Prat 1993 Jan 15;43(2):146-51
The role played by zinc in biology is now better known, and numerous
biochemical mechanisms, such as immunity or actions on several hormones
and more than 200 enzymes, have proved to be zinc-dependent. Thus, many
functions are disturbed when this trace metal is deficient, including,
for example, taste and appetite, cell multiplication, growth, pregnancy,
fertility, defence against bacteria and brain functions. Zinc intake has
been found to be unexcessive and indeed, at the limit of sufficiency in
the French population. Groups at risk, such as neonates, growing children,
pregnant women and elderly people, should have a higher zinc intake provided
by dietary measures or supplementation. Zinc supplementation has been
shown to exert a beneficial effect in randomized studies concerning children's
growth, acne, old people's immunity or low female fertility. Such supplementation
must be balanced and given in moderate doses since zinc interacts with
other foodstuffs, and an excess of zinc can be as bad as its deficiency
in our nutrition.
11. Effects of oral zinc and vitamin A in acne.
Michaelsson G, Juhlin L, Vahlquist A
Arch Dermatol 1977 Jan;113(1):31-6
The effects of oral zinc sulfate (corresponding to 135 mg of zinc daily)
alone and in combination with vitamin A (300,000 international units)
daily on acne lesions have been compared with those of vitamin A alone
and of a placebo. The number of comedones, papules, pustules, and infiltrates
were counted at each visit. After four weeks, there was a significant
decrease in the number of papules, pustules, and infiltrates in the zinc-treated
groups. The effect of zinc plus vitamin A was not better than zinc alone.
After 12 weeks of treatment, the mean acne score had decreased from 100%
to 15%. The mechanism for the effect of zinc therapy in acne, to our knowledge,
is not presently known.
12. Serum zinc and retinol-binding protein in acne.
Michaelsson G, Vahlquist A, Juhlin L
Br J Dermatol 1977 Mar;96(3):283-6
The serum levels of zinc and retinol-binding protein (RBP) have been
determined in 173 patients with acne and compared with those of a control
group. The RBP is a specific transport protein and its level in plasma
reflects the amount of vitamin A available to the tissues. Patients with
severe acne were found to have lower levels of RBP than either patients
with mild acne or healthy subjects of the same age. In the case of males
with severe acne, the mean serum zinc level was significantly lower than
that of the control group. No such difference was observed for girls.
The observed condition of low levels of zinc and vitamin A in the serum
of patients with severe acne may provide a rationale for the clinically
good effect of oral zinc treatment.
13. A double-blind controlled evaluation of the sebosuppressive activity
of topical erythromycin-zinc complex.
Pierard-Franchimont C, Goffin V, Visser JN, Jacoby H, Pierard GE Department
of Dermatopathology, University of Liege, Belgium.
Eur J Clin Pharmacol 1995;49(1-2):57-60
In a double-blind randomised study, 14 volunteers applied 4% erythromycin
plus 1.2% zinc (Zineryt lotion) and 4% erythromycin lotions, each on half
of the forehead twice daily for 3 months. The sebum output was evaluated
at 3-week intervals using the photometric and the lipid-sensitive film
methods. Evaluations of casual level (CL) and sebum excretion rate (SER)
were made with a Sebumeter, and total area of lipid spots (TAS) was measured
on Sebutapes. Compared to baseline values, the formulation of the erythromycin-zinc
complex induced significant reductions in SER after 6 and 9 weeks, and
in CL and TAS at 3, 6, 9 and 12 weeks. The mean reduction in TAS was over
20% for four successive 1-h samplings on completion of the study. Significant
reductions in CL, SER and TAS were observed for the erythromycin-zinc
formulation compared to the control lotion at 6 and 9 weeks, and also
at 3 weeks for SER and TAS, and at 12 weeks for CL and TAS. This study
indicates that sebum output is significantly reduced by the erythromycin-zinc
complex. This reduction is theoretically beneficial for the acneic patient.
ADD – ADHD
14. Does zinc moderate essential fatty acid and amphetamine treatment
of attention-deficit/hyperactivity disorder?
Arnold LE, Pinkham SM, Votolato N. Department of Psychiatry, Ohio State
University, Columbus, USA. Arnold.6@osu.edu
J Child Adolesc Psychopharmacol 2000 SUMMMER;10(2):111-7
Zinc is an important co-factor for metabolism relevant to neurotransmitters,
fatty acids, prostaglandins, and melatonin, and indirectly affects dopamine
metabolism, believed intimately involved in attention-deficit/hyperactivity
disorder (ADHD). To explore the relationship of zinc nutrition to essential
fatty acid supplement and stimulant effects in treatment of ADHD, we re-analyzed
data from an 18-subject double-blind, placebo-controlled crossover treatment
comparison of d-amphetamine and Efamol (evening primrose oil, rich in
gamma-linolenic acid). Subjects were categorized as zinc-adequate (n =
5), borderline zinc (n = 5), and zinc-deficient (n = 8) by hair, red cell,
and urine zinc levels; for each category, placebo-active difference means
were calculated on teachers' ratings. Placebo-controlled d-amphetamine
response appeared linear with zinc nutrition, but the relationship of
Efamol response to zinc appeared U-shaped; Efamol benefit was evident
only with borderline zinc. Placebo-controlled effect size (Cohen's d)
for both treatments ranged up to 1.5 for borderline zinc and dropped to
0.3-0.7 with mild zinc deficiency. If upheld by prospective research,
this post-hoc exploration suggests that zinc nutrition may be important
for treatment of ADHD even by pharmacotherapy, and if Efamol benefits
ADHD, it likely does so by improving or compensating for borderline zinc
nutrition.
CARDIOVASCULAR DISEASE
15. Emerging concepts of neurohumoral modulation in the treatment of
congestive heart failure.
Mulder P, Thuillez Ch.
INSERM E9920, IFRMP No. 23, Rouen University Medical School, France.
paul.mulder@univ-rouen.fr
Arch Mal Coeur Vaiss. 2002 Sep;95(9):821-6.
The angiotensin converting enzyme (ACE), endothelin (ET) converting enzyme
(ECE) and neutral endopeptidase (NEP) are all zinc-metallopeptidases expressed
in almost all the organs, such as heart, vessels and kidneys. While ACE
and ECE are respectively involved in the transformation of angiotensin
I and Big-ET into angiotensin II and ET-1 respectively, which possess
vasoconstrictor and mitogenic properties, NEP is involved in the degradation
of atrial natriuric
factor (ANF), which possesses vasorelaxant, diuretic/natriuretic and
antihypertrophic properties. These three systems are activated in heart
failure
and modulate the progression of heart failure. This article will discuss
preliminary date concerning simultaneous inhibition of ACE, ECE and/or
NEP and their therapeutic potential interest in the treatment of heart
failure.
16. Magnesium and zinc status in survivors of sudden unexplained death
syndrome in northeast Thailand.
Pansin P, Wathanavaha A, Tosukhowong P, Sriboonlue P, Tungsanga K, Dissayabutr
T, Tosukhowong T, Sitprija V.
Department of Internal Medicine, Faculty of Medicine, Chulalongkorn University,
Bangkok, Thailand.
Southeast Asian J Trop Med Public Health. 2002 Mar;33(1):172-9.
Sudden Unexplained Death Syndrome (SUDS) is a major health problem in
rural
residents of Northeast Thailand. The cause of death in SUDS is suspected
to be
cardiovascular abnormalities. As magnesium (Mg) and zinc (Zn) deficiency
contribute significantly to several cardiovascular diseases, we investigated
the
Mg- and Zn-status of patients with sudden respiratory distress and cardiac
arrest who had survived resuscitation attempts or a near-SUDS episode
(N-SUDS). The following subjects were enrolled: 12 N-SUDS inhabitants
of rural Northeast Thailand (rural group 1, R1), 13 rural villagers with
no past history of N-SUDS (rural group 2, R2), 15 urban Northeasterners
(urban group 1, U1); 13
Bangkokians (urban group 2, U2). All subjects were free of structural
heart
disease. Magnesium and zinc were assessed by atomic absorption spectrophotometry
of samples of plasma, red blood cells (RBC), white blood cells (WBC),
and 24-hour urine. The mean levels of magnesium in the RBC, WBC, and 24-hour
urine of N-SUDS patients (R1) were significantly lower than those of the
urban groups (U1 and U2), while the plasma levels did not show any differences.
When comparing the Zn-status of R1 with that of the urban groups (U1 and
U2), the plasma, RBC, and WBC levels were found to be significantly lower
in R1 (except for the RBC-Zn of the U1 group), while the 24-hour urine
levels was higher. Although the magnesium and zinc parameters were not
significantly different between the rural groups R1 and R2, the prevalence
of hypomagnesuria (<2.2 mmol/day), hypozincemia (<9.7 micromol/l),
and hyperzincuria (>10.7 micromol/day) was higher in the R1 group.
These findings suggest that the homeostasis of both magnesium and zinc
is altered in N-SUDS patients. Similar alterations, to a lesser degree,
were observed in those people living in the same rural environment (R2).
17. Analysis of ionic ratios in myocardial tissue and their relation
to cardiac
damage.
Torres MC, Osuna E, Perez-Carceles MD, Gomez-Zapata M, Luna A.
Institute of Forensic Medicine of Murcia, Spain.
Am J Forensic Med Pathol. 2002 Jun;23(2):155-8.
The authors evaluated the usefulness of the postmortem biochemical analysis
of
ionic ratios in different parts of the heart and their relation to cardiac
damage caused by chest trauma, as observed by anatomopathologic study.
Fifty-nine 59 cases were studied, selected from routine necropsies, and
samples
were taken from different sites of cardiac tissue. The cause of death
was trauma
in 40 cases and nontraumatic causes in 19 cases. The object of this study
was to
analyze the levels of Na+, K+, Ca+2, Mg+2, and Zn+2 in different zones
of the
heart, and the relationship between intracellular and extracellular ion
ratios
and the different causes of death and any anatomopathologic alterations
observed. The biochemical tests revealed a possible relation between the
ionic
values and cause of death. Alterations in cell membrane permeability and
corresponding modification of the ionic ratios were produced earlier than
histologic alterations, which need longer to establish themselves whether
or not
they follow a traumatic process.
18. Influence of zinc on cardiac and serum biochemical parameters in
rabbits.
Bhaskar M, Madhuri E, Abdul Latheef SA, Subramanyam G.
Department of Zoology, S.V. University Post Graduate Centre, Kavali, India.
Indian J Exp Biol. 2001 Nov;39(11):1170-2.
The pattern of lipid profiles and organic constituents of cardiac and
serum
tissues of rabbits were studied on treatment with cholesterol, zinc and
zinc +
cholesterol. Total carbohydrate and total protein levels were decreased
with
elevated lipid levels in cholesterol fed rabbits. However, the zinc and
cholesterol + zinc fed rabbits showed decreased lipid fractions in cardiac
and
serum tissues leading to reduced atherosclerotic process in rabbits. These
results suggest that the zinc is acting as a hypolipidaemic and anti atherogenic
agent in experimental rabbits.
19. Diagnostic and therapeutic potential of the endothelin system in
patients with chronic heart failure.
Krum H, Denver R, Tzanidis A, Martin P.
Clinical Pharmacology Unit, Dept of Epidemiology & Preventive
Medicine/Department of Medicine, Monash University/Alfred Hospital, Prahran,
Victoria, Australia. henry.krum@med.monash.edu.au
Heart Fail Rev. 2001 Dec;6(4):341-52.
There is now considerable evidence to support a role for the endothelin
(ET)
system in the pathogenesis and progression of chronic heart failure (CHF).
As
such, the potential exists for this system to be useful in both diagnosis
(by
measurement of peptide levels in plasma and other body fluids) and treatment
(by pharmacological blockade) of this condition.Plasma levels of endothelin-1
(ET-1) are elevated in CHF and the magnitude of elevation correlates with
disease severity. ET-1 levels in plasma predict subsequent mortality in
patients with CHF. ET-1 may also contribute to symptoms associated with
CHF, such as exercise intolerance. In the diagnosis of CHF, plasma levels
of ET-1 appear to be a less powerful discriminator between patients with
mild disease and control subjects with normal ventricular function on
multivariate analyses, compared to brain natriuretic peptide (BNP), or
its N-terminal fragment. ET-1 concentrations are also elevated in the
saliva of patients with CHF and may represent an
alternative approach to assessment of the status of the ET system in these
patients.Specific ET receptor antagonists (both mixed and ET(A)-selective)
have
been developed. Studies with these agents in animal models of CHF have
demonstrated beneficial effects via both haemodynamic and non-haemodynamic
pathways. A number of short-term clinical studies have been performed
demonstrating improvements in haemodynamic parameters without neurohormonal
activation. Long-term clinical studies with ET receptor antagonists are
currently underway to definitively test the impact of blockade of this
system on mortality and major cardiovascular endpoints. Endothelin converting
enzyme (ECE) inhibitors represent an alternative strategy of ET blockade,
and early data from animal models suggest these agents may be of clinical
utility, either alone or, more likely, in combination with other zinc
metallopeptidases.
20. Antioxidant status in cerebrovascular accident.
Kocaturk PA, Akbostanci MC, Isikay C, Ocal A, Tuncel D, Kavas GO, Mutluer
N.
Departments of Pathophysiology, Faculty of Medicine, Ankara University,
Sihhiye, Turkey.
Biol Trace Elem Res. 2001 May;80(2):115-24.
Ischemia is associated with the pathological changes caused by the accumulation
of reactive oxygen metabolites (ROM) in cerebrovascular accident (CVA).
The aim of this study was to determine red cell copper/zinc-superoxide
dismutase (Cu/Zn-SOD) and catalase activities and copper and zinc concentrations
both in plasma and in red cells in CVA. Cu/Zn-SOD and catalase activities
of 16 patients, with an average age of 64 yr, were measured spectrophotometrically;
copper and zinc concentrations were determined by atomic absorption spectrophotometer.
The results showed that Cu/Zn-SOD activity was increased markedly in patients
compared to the young controls and reached a peak on the d 5 of the disease,
whereas the catalase activity of the patients on d 3 and d 5 were in the
normal range, but higher on d 10. The enzyme activities of the elderly
group were generally increased compared to the young controls. Copper
and zinc concentrations showed corresponding alterations. These findings
suggested that the effects of oxidative stress in CVA might be reflected
in red cell and plasma parameters.
21. Nutritional factors in the pathobiology of human essential hypertension.
Das UN.
EFA Sciences LLC, Norwood, Massachusetts 02062, USA. undurti@hotmail.com
Nutrition. 2001 Apr;17(4):337-46.
Endothelial cells produce vasodilator and vasoconstrictor substances.
Dietary
factors such as sodium, potassium, calcium, magnesium, zinc, selenium,
vitamins A, C, and E, and essential fatty acids and their products such
as eicosanoids can influence blood pressure, cardio- and cerebrovascular
diseases, and concentrations of blood lipids and atherosclerosis. There
might be a close
interaction between these dietary factors, sympathetic and parasympathetic
nervous systems, the metabolism of essential fatty acids, nitric oxide,
prostacyclin, and endothelium in human essential hypertension. A deficiency
in
any one factor, dietary or endogenous, or alterations in their interactions
with
each other, can lead to endothelial dysfunction and development of hypertension.
Therefore, alterations in the metabolism of essential fatty acids might
be a
predisposing factor to the development of essential hypertension and insulin
resistance.
22. Cardiovascular risk factors in relation to the serum concentrations
of copper and zinc: epidemiological study on children and adolescents
in the Spanish province of Navarra.
Elcarte Lopez T, Villa Elizaga I, Gost Garde JI, Elcarte Lopez R, Martin
Perez
A, Navascues Pujada J, Navarro Blasco I, Aparicio Madre MI.
Primary Health Care Center, Pamplona, Navarra, Spain.
Acta Paediatr. 1997 Mar;86(3):248-53.
This investigation was carried out to show the possible association between
groups of children with extreme values of copper and zinc concentrations
and
cardiovascular risk indicators. Serum copper and zinc concentrations were
analysed in a group of 3887 children from Navarra, Spain (both sexes.
aged 4-17
years). Hypertension, unfavourable serum lipid profile (total cholesterol,
high
density lipoprotein cholesterol, low density lipoprotein cholesterol,
triglycerides, and cholesterol/HDL and LDL/HDL ratios), and degree of
adiposity (weight, height, subcutaneous skinfolds, Quetelet's index and
mean of subcutaneous skinfolds) were evaluated. Positive correlation was
found between several lipid parameters and copper and zinc concentrations,
i.e. degree of correlation related with age, except for copper/HDL and
triglycerides/zinc ratios, where correlation remained negative at all
points. Copper levels were correlated with adiposity parameters in an
age-dependent fashion (Quetelet's index: r = 0.01 for ages 4-7 years to
r = 0.10, p < 0.01 for ages 14-17 years; mean skinfold thickness: r
= 0.05 for ages 4-7 years up to r = 0.18, p < 0.01 for ages 14-17 years).
Most correlations between lipid parameters and copper and zinc are markedly
amplified if adiposity parameters are taken into account. However, the
only significant association was the established relation between high
copper concentrations (> x + 2SD) and unfavourable serum lipid profile(LDL/HDL
> 2.2).
23. Serum calcium, magnesium, copper and zinc and risk of cardiovascular
death.
Reunanen A; Knekt P; Marniemi J; Maki J; Maatela J; Aromaa A
National Public Health Institute, Helsinki, Finland.
Eur J Clin Nutr (England) Jul 1996, 50 (7) p431-7
OBJECTIVE: To study the association of serum calcium, magnesium, copper
and zinc concentrations with cardiovascular mortality.
DESIGN: A nested case-control study within a prospective population study.
SUBJECTS AND METHODS: 230 men dying from cardiovascular diseases and 298
controls matched for age, place of residence, smoking and follow-up time.
Mean follow-up time was 10 years. Serum calcium, magnesium, copper and
zinc concentrations were determined from samples kept frozen at -20 degrees
C.
RESULTS: High serum copper and low serum zinc concentrations were significantly
associated with an increased mortality from all cardiovascular diseases
and from coronary heart disease in particular. The relative risk of coronary
heart disease mortality between the highest and lowest tertiles of serum
copper and zinc were 2.86 (P = 0.03) and 0.69 (P = 0.04), respectively.
Adjustment for social class, serum cholesterol, body mass index, hypertension
and known heart disease at baseline examination did not materially alter
the results. No significant differences were observed in concentrations
of serum calcium and magnesium between cases and controls. CONCLUSIONS:
High serum copper and low serum zinc are associated with increased cardiovascular
mortality whereas no association was found with serum calcium and magnesium
and mortality risk.
COMMON COLD
24. Zinc lozenges reduce the duration of common cold symptoms.
ANON [No Authors Listed]
Nutr Rev (United States) Mar 1997, 55 (3) p82-5
A randomized, double-blind, placebo-controlled clinical trial has shown
that treatment of the common cold with zinc gluconate lozenges resulted
in a significant reduction in duration of symptoms of the cold. Patients
received zinc-containing lozenges or placebo lozenges every 2 hours for
the duration of cold symptoms. The median time to complete resolution
of cold symptoms was 4.4 days in the zinc group compared with 7.6 days
in the placebo group. The mechanism of action of zinc in treating the
common cold remains unknown. (13 Refs.)
25. Zinc gluconate lozenges for treating the common cold. A randomized,
double-blind, placebo-controlled study
Mossad SB; Macknin ML; Medendorp SV; Mason P Cleveland Clinic Foundation,
Ohio, USA.
Ann Intern Med (United States) Jul 15 1996, 125 (2) p81-8, Comment in
Ann Intern Med 1996 Jul 15;125(2):142-4
BACKGROUND. The common cold is one of the most frequent human illnesses
and is responsible for substantial morbidity and economic loss. No consistently
effective therapy for the common cold has been well documented, but evidence
suggests that several possible mechanisms may make zinc an effective treatment.
OBJECTIVE. To test the efficacy of zinc gluconate lozenges in reducing
the duration of symptoms caused by the common cold. DESIGN. Randomized,
double-blind, placebo-controlled study. SETTING. Outpatient department
of a large tertiary care center. PATIENTS. 100 employees of the Cleveland
Clinic who developed symptoms of the common cold within 24 hours before
enrollment. INTERVENTION. Patients in the zinc group (n = 50) received
lozenges (one lozenge every 2 hours while awake) containing 13.3 mg of
zinc from zinc gluconate as long as they had cold symptoms. Patients in
the placebo group (n = 50) received similarly administered lozenges that
contained 5% calcium lactate pentahydrate instead of zinc gluconate. MAIN
OUTCOME MEASURES. Subjective daily symptom scores for cough, headache,
hoarseness, muscle ache, nasal drainage, nasal congestion, scratchy throat,
sore throat, sneezing, and fever (assessed by oral temperature). RESULTS.
The time to complete resolution of symptoms was significantly shorter
in the zinc group than in the placebo group (median, 4.4 days compared
with 7.6 days; P < 0.001). The zinc group had significantly fewer
days with coughing (median, 2.0 days compared with 4.5 days; P = 0.04),
headache (2.0 days and 3.0 days; P = 0.02), hoarseness (2.0 days and 3.0
days; P = 0.02), nasal congestion (4.0 days and 6.0 days; P = 0.002),
nasal drainage (4.0 days and 7.0 days; P < 0.001), and sore throat
(1.0 day and 3.0 days; P < 0.001). The groups did not differ significantly
in the resolution of fever, muscle ache, scratchy throat, or sneezing.
More patients in the zinc group than in the placebo group had side effects
(90% compared with 62%; P < 0.001), nausea (20% compared with 4%;
P = 0.02), and bad-taste reactions (80% compared with 30%; P <
0.001),
CONCLUSION. Zinc gluconate in the form and dosage studied significantly
reduced the duration of symptoms of the common cold. The mechanism of
action of this substance in treating the common cold remains unknown.
Individual patients must decide whether the possible beneficial effects
of zinc gluconate on cold symptoms outweigh the possible adverse effects.
DIABETES
26. Decreased serum magnesium and zinc levels: atherogenic implications
in type-2 diabetes mellitus in Nigerians.
Anetor JI, Senjobi A, Ajose OA, Agbedana EO.
Department of Chemical Pathology, College of Medicine, University College
Hospital, Ibadan, Nigeria.
Nutr Health. 2002;16(4):291-300.
Serum magnesium, zinc and total cholesterol were evaluated in 40 Nigerian
patients suffering from type-2 diabetes mellitus (21M, 19F) and 20 (14M,
6F)
apparently normal non diabetic control subjects. The mean age of the diabetic
patients was similar to that of controls (p > 0.05). The mean duration
of the
disease was (4.7 + 0.7 SEM) in these patients. Fasting blood glucose and
total
cholesterol were significantly higher in diabetics than in non diabetic
control
subjects (p > 0.001). The serum total cholesterol showed inter-group
variation
when the patients were classified into four different age groups. In contrast,
the serum level of magnesium (Mg) and zinc (Zn) were significantly lower
in
diabetics than in controls (p > 0.001). There were no significant correlation
between glucose and the minerals, Mg. and Zn. Serum total cholesterol
showed a significant positive correlation with magnesium (r = 0.6: p >
0.001), while the
correlation with zinc was not significant. In type-2 diabetic mellitus
the
concentration of both Mg and Zn levels were significantly reduced, probably
suggesting lower antioxidant status in this condition. The implication
is the
greater susceptibility to LDL-cholesterol oxidation. The attendant risk
of
development of premature Coronary Heart Disease is discussed. Magnesium
and zinc are nutritional minerals that play crucial roles in the regulation
of
carbohydrate and lipid metabolism.
27. Dietary zinc supplementation inhibits NFkappaB activation and protects
against chemically induced diabetes in CD1 mice.
Ho E, Quan N, Tsai YH, Lai W, Bray TM. Department of Human Nutrition,
The Ohio State University, Columbus 43210, USA.
Exp Biol Med (Maywood) 2001 Feb;226(2):103-11
Zinc status in patients with Type I diabetes is significantly lower than
healthy controls. Whether zinc supplementation can prevent the onset of
Type I diabetes is unknown. Recent studies have suggested that the generation
of reactive oxygen species (ROS) is a cause of beta cell death leading
to Type I diabetes. In addition, we found that activation of NFkappaB
(a ROS-sensitive transcription factor that regulates immune responses)
may be the key cellular process that bridges oxidative stress and the
death of beta cells. Zinc is a known antioxidant in the immune system.
Therefore, this study is designed to test whether an increase in dietary
zinc can prevent the onset of Type I diabetes by blocking NFkappaB activation
in the pancreas. The results show that high zinc intake significantly
reduced the severity of Type I diabetes (based on hyperglycemia, insulin
level, and islet morphology) in alloxan and streptozotocin-induced diabetic
models. Zinc supplementation also inhibited NFkappaB activation and decreased
the expression of inducible NO synthase, a downstream target gene of NFkappaB.
It is concluded that zinc supplementation can significantly inhibit the
development of Type I diabetes. The ability of zinc to modulate NFkappaB
activation in the diabetogenic pathway may be the key mechanism for zinc's
protective effect. Inhibition of the NFkappaB pathway may prove to be
an important criterion for choosing nutritional strategies for Type I
diabetes prevention.
28. Oral zinc therapy in diabetic neuropathy.
Gupta R, Garg VK, Mathur DK, Goyal RK.
Dept. of Medicine, JLN Medical College and Associated Group of Hospital,
Ajmer, Rajasthan-305 001.
J Assoc Physicians India. 1998 Nov;46(11):939-42.
The present double blind randomized study was conducted on 50 subjects;
20 age and sex matched healthy controls (Group--I); 15 patients of diabetes
mellitus
with neuropathy who received placebo for 6 weeks (Group--IIA); and 15
patients
of diabetes mellitus with neuropathy who were given supplemental zinc
sulphate
(660 mg) for 6 weeks (Group--IIB). Serum zinc level, fasting blood sugar
(FBS)
and post prandial blood sugar (PPBS) levels and motor nerve conduction
velocity
(MNCV) were estimated on day 0 and after 6 weeks in all subjects. Serum
zinc
levels were significantly low (p < 0.001) in group IIA and IIB as compared
to
healthy controls (Group--I) at baseline. After 6 weeks the change in pre
and
post therapy values of FBS, PPBS and MNCV (median and common peroneal
nerve) were highly significant (P = < 0.001) for group IIB alone with
insignificant
change (P = > 0.05) in group IIA. No improvement (P = > 0.05) in
autonomic
dysfunction was observed in either groups. Therefore, oral zinc supplementation
helps in achieving better glycemic control and improvement in severity
of
peripheral neuropathy as assessed by MNCV.
29. [Low zinc levels in metabolic X syndrome (mzX) patients measured
by hair zinc composition analysis] [Article in Polish]
Lukasiak J, Cajzer D, Dabrowska E, Falkiewicz B.
Pracownia Analizy Instrumentalnej, Katedra Chemii Fizycznej AM w Gdansku.
Rocz Panstw Zakl Hig. 1998;49(2):241-4.
The hair zinc content in 16 patients with metabolic X syndrome (mzX)
was
measured by means of atomic absorption spectrometry method. The mean
concentration (125.13 mg/kg) was lower than in the majority of other published
studies. The differences among groups of patients with different sex or
diseases
(e.g. coronary heart disease, hypertension, type II diabetes mellitus)
were not
significant. It seems to be probably that deficiency of zinc plays a role
in
pathogenesis of mzX or that it is a consequence of mzX.
30. [Influence of insufficient zinc on immune functions in NIDDM patients]
[Article in Chinese]
Wang P, Yang Z.
Department of Endocrinology, Second Affiliated Hospital, Hunan Medical
University, Changsha.
Hunan Yi Ke Da Xue Xue Bao. 1998;23(6):599-601.
The serum zinc level and immune functions were analyzed in 34 patients
with
NIDDM before and after the treatment with zinc gluconate supplement during
conventional therapy (after the blood glucose level stabilization). The
results
showed that before treatment the level of serum zinc and red cell C3b
receptor
rosette(RBCK-C3b RR), T-lymphocyte subgroup CD3, CD4, and CD4/CD8 were
decreased(P < 0.01), while CD8, red cell immune complex rosette(RBC-ICR)
were increased. After treatment with zinc gluconate for 1 month the serum
zinc level, RBC-C3b RR, RBC-ICR, CD3 and CD4/CD8 became normal, CD8 also
approached to normal. All the above figures were significantly different
before and after zinc therapy. The data showed that various degrees of
lowering of serum zinc and abnormal immune functions were present during
the conventional antidiabetic therapy. Thus, zinc supplement should be
used as an important adjunctive therapy for NIDDM patients.
31. Hyperzincuria in individuals with insulin-dependent diabetes mellitus:
concurrent zinc status and the effect of high-dose zinc supplementation.
Cunningham JJ, Fu A, Mearkle PL, Brown RG.
Department of Nutrition, University of Massachusetts, Amherst, MA 01003-1420.
Metabolism 1994 Dec;43(12):1558-62
The urinary excretion of zinc in individuals with insulin-dependent diabetes
mellitus (IDDM) is approximately doubled. In the absence of a compensatory
mechanism, this hyperzincuria should induce a deficient or marginal Zn
status. We examined parameters of Zn status in plasma and in blood cells
with respect to urinary Zn losses and Zn supplementation. We measured
Zn levels in the urine, plasma, and erythrocytes of 14 IDDM subjects and
15 nondiabetics who kept dietary records for 3 consecutive days. Subsequently,
six IDDM subjects and seven nondiabetics were supplemented with 50 mg
Zn daily for 28 days. We measured the above parameters, as well as mononuclear
leukocyte Zn (MNL-Zn) and the plasma subfraction of albumin-bound Zn (alb-Zn).
The total plasma Zn-binding capacity was also assessed. Plasma copper
and erythrocyte Cu were monitored as indicators of potential Zn toxicity.
Individuals with IDDM displayed the expected hyperzincuria, but had normal
blood Zn parameters. Zincuria increased by a similar amount in both groups
during supplementation, as did the MNL-Zn content. However, erythrocyte
Zn (e-Zn) was refractory, so a trend toward lower e-Zn among IDDM subjects
persisted during Zn supplementation. Hemoglobin A1c (HbA1c) increased
markedly in the Zn-supplemented IDDM group. Despite their chronic hyperzincuria,
individuals with IDDM appear not to be Zn-deficient. Large-dose Zn supplementation
increases MNL-Zn and induces an undesirable elevation of HbA1c in all
individuals. This is especially disconcerting for those with IDDM, and
may reflect an exacerbation of a chronic "Zn diabetes." These
data suggest a potential for toxicity from large-dose Zn supplementation.
32. Zinc and insulin sensitivity.
Faure P, Roussel A, Coudray C, Richard MJ, Halimi S, Favier A.
Laboratoire de Biochimie C, Hopital A. Michallon, Grenoble, France.
Biol Trace Elem Res 1992 Jan-Mar;32:305-10
Many studies have shown that zinc deficiency could decrease the response
to insulin. In genetically diabetic animals, a low zinc status has been
observed contrary to induced diabetic animals. The zinc status of human
patients depends on the type of diabetes and the age. Zinc supplementation
seems to have beneficial effects on glucose homeostasis. However, the
mechanism of insulin resistance secondary to zinc depletion is yet unclear.
More studies are therefore necessary to document better zinc metabolism
in diabetes mellitus, and the antioxidant activity of zinc on the insulin
receptor and the glucose transporter.
33. The influence of zinc supplementation on glucose homeostasis in NIDDM.
Raz I, Karsai D, Katz M.
Department of Medicine B, Hadassah University Hospital, Ein Karem, Israel.
Diabetes Res 1989 Jun;11(2):73-9
Decreased serum zinc levels and hyperzincuria occur in some non-insulin
dependent diabetic subjects (NIDDM). Zinc deficiency was demonstrated
in various tissues of animal models for NIDDM. Serum zinc and 24-hr urine
zinc of subjects with NIDDM were compared with that of age- and sex-matched
healthy volunteers. Zincuria was significantly increased in the diabetic
group. Thirteen diabetic subjects with hyperzincuria and hypozincemia
were supplemented with zinc sulfate 220 mg x 3/day for 7-8 weeks. At the
end of the study, glucose disposal (evaluated by kg) decreased significantly
from 0.562 +/- 0.03 to 0.414 +/- 0.05 (p less than 0.05) and fasting glucose
and fructosamine were significantly increased from 177 +/- 10 mg/dl to
207 +/- 15 mg/dl (p less than 0.05) and from 2.7 +/- 0.2% to 3.2 +/- 0.28%
(p less than 0.05), respectively. T-lymphocyte response to phytohemagglutinin
was increased significantly. We conclude that zinc supplementation to
NIDD patients with hypozincemia and hyperzincemia might aggravate their
glucose intolerance. More accurate methods to assess zinc deficiency in
NIDD patients is needed to justify the supplementation of zinc in these
patients.
ELDERLY
34. Zinc and immunoresistance to infection in aging: new biological tools.
Mocchegiani E, Muzzioli M, Giacconi R.
Immunology Centre, Research Department 'Nino Masera', Italian National
Research Centres on Aging (I.N.R.C.A.), Via Birarelli 8, 60121, Ancona,
Italy.
e.mocchegiani@inrca.it
Trends Pharmacol Sci. 2000 Jun;21(6):205-8.
Comment in:
Trends Pharmacol Sci. 2001 Mar;22(3):112-3.
Infections can cause mortality when the immune system is damaged. The
catalytic, structural (in zinc-finger proteins) and regulatory roles of
zinc mean that this ion is involved in the maintenance of an effective
immune response. Both zinc deficiency and impaired cell-mediated immunity
combine during aging to result in increased susceptibility to infection.
Dietary supplementation with the
recommended daily allowance of zinc for between one and two months decreases
the incidence of infection and increases the survival rate following infection
in the elderly. This article reviews the biochemical pathways through
which zinc might act to increase immunoresistance to infection in the
elderly.
35. Zinc and copper intakes and their major food sources for older adults
in the 1994-96 continuing survey of food intakes by individuals (CSFII).
Ma J, Betts NM.
Department of Nutritional Science and Dietetics, University of Nebraska,
Lincoln, NE 68583, USA.
J Nutr. 2000 Nov;130(11):2838-43.
Full text article
http://www.nutrition.org/cgi/content/full/130/11/2838
Zinc and copper are two trace minerals essential for important biochemical
functions and necessary for maintaining health throughout life. Several
national
food surveys revealed marginally to moderately low contents of both nutrients
in
the typical American diet. Using data from the respondents >/= 60 y
old in the
1994-96 Continuing Survey of Food Intakes by Individuals (CSFII), we examined
average dietary intakes of zinc, copper and relevant dietary factors;
primary
dietary contributors of zinc and copper; and Zn:Cu ratios of the primary
dietary
contributors. Data were analyzed with the use of a chi(2) test, Student's
t test
and multivariate analysis of covariance with Bonferroni correction. The
daily
zinc intake was 12 +/- 6.4 mg for men and 8.0 +/- 4.0 mg for women (P
< 0.05);
the daily copper intake was 1.3 +/- 0.7 mg for men and 1.0 +/- 0.5 mg
for women
(P < 0.05). Foods such as beef, ground beef, legumes, poultry, ready-to-eat
and
hot cereals, and pork constituted the major sources of zinc. Copper consumption
was contributed mainly by legumes, potato and potato products, nuts and
seeds,
and beef. The less-than-recommended intakes of zinc and copper by the
elderly
were likely associated with age, low income and less education. The intakes
of
zinc and copper could be improved by more frequent consumption of food
sources rich in these minerals. An inherent limitation of this study was
the use of the 24-h dietary recall method, which may underestimate usual
dietary intakes.
Nonetheless, this study affirms the need for assessment of zinc and copper
nutriture in the elderly.
36. [Zinc: pathophysiological effects, deficiency status and effects
of supplementation in elderly persons--an overview of the research]
[Article in German]
Abbasi A, Shetty K.
Medical College of Wisconsin, Milwaukee 53226, USA.
Z Gerontol Geriatr. 1999 Jul;32 Suppl 1:I75-9.
Zinc is an essential micronutrient. Several studies have shown that zinc
deficiency is common in older people. Zinc has been extensively studied
with
regard to its role in wound healing, infections, immune system, cardiovascular
disease, and several other medical conditions. Several investigators have
published intervention studies using zinc supplements in older people
with
favorable outcomes. This paper will briefly review the pathophysiologic
effects
of zinc, nutritional deficiency, and effects of zinc supplementation in
older
people.
37. Impact of trace elements and vitamin supplementation on immunity
and infections in institutionalized elderly patients: a randomized controlled
trial. MIN. VIT. AOX. geriatric network.
Girodon F, Galan P, Monget AL, Boutron-Ruault MC, Brunet-Lecomte P, Preziosi
P, Arnaud J, Manuguerra JC, Herchberg S.
Scientific and Technical Institute for Foods and Nutrition, Conservatiore
National des Arts et Mettiers, Paris, France.
Arch Intern Med. 1999 Apr 12;159(7):748-54.
BACKGROUND: Antioxidant supplementation is thought to improve immunity
and thereby reduce infectious morbidity. However, few large trials in
elderly people have been conducted that include end points for clinical
variables. OBJECTIVE: To determine the effects of long-term daily supplementation
with trace elements (zinc sulfate and selenium sulfide) or vitamins (beta
carotene, ascorbic acid, and vitamin E) on immunity and the incidence
of infections in institutionalized elderly people. METHODS: This randomized,
double-blind, placebo-controlled intervention study included 725 institutionalized
elderly patients (>65 years) from 25 geriatric centers in France. Patients
received an oral daily supplement of nutritional doses of trace elements
(zinc and selenium sulfide) or vitamins (beta carotene, ascorbic acid,
and vitamin E) or a placebo within a 2 x 2 factorial design for 2 years.
MAIN OUTCOME MEASURES: Delayed-type hypersensitivity skin response, humoral
response to influenza vaccine, and infectious morbidity and mortality.
RESULTS: Correction of specific nutrient deficiencies was observed after
6 months of supplementation and was maintained for the first year, during
which there was no effect of any treatment on delayed-type hypersensitivity
skin response. Antibody titers after influenza vaccine were higher in
groups that received trace elements alone or associated with vitamins,
whereas the vitamin group had significantly lower antibody titers (P<.05).
The number of patients without respiratory tract infections during the
study was higher in groups that received trace elements (P = .06). Supplementation
with neither trace elements nor vitamins significantly reduced the incidence
of urogenital infections. Survival analysis for the 2 years did not show
any differences between the 4 groups. CONCLUSIONS: Low-dose supplementation
of zinc and selenium provides significant improvement in elderly patients
by increasing the humoral response after vaccination and could have considerable
public health importance by reducing morbidity from respiratory tract
infections.
38. [Diagnosis of zinc deficiency] [Article in German]
Roth HP, Kirchgessner M.
Institut fur Ernahrungsphysiologie, Technischen Universitat Munchen.
Z Gerontol Geriatr. 1999 Jul;32 Suppl 1:I55-63.
Though far more common, particularly in elderly people, than was previously
assumed, marginal zinc deficiency does not lead to the classical manifestations
of zinc deficiency and is therefore difficult to diagnose. There is therefore
a
need for sensitive parameters that can reliably demonstrate even marginal
zinc
deficiency, as suboptimal zinc status can seriously impair human health,
performance, reproductive functions, and mental and physical development.
The
most important criteria for the diagnosis of zinc deficiency are critically
discussed. The laboratory parameters currently considered to be the most
useful
indicators of marginal zinc deficiency are zinc-binding capacity and
serum/plasma alkaline phosphatase activity before and after zinc supplementation
(zinc tolerance test!). In order to obtain a reliable assessment of a
patients zinc status, a number of different diagnostic parameters should
always be measured.
39. Effect of micronutrient supplementation on infection in institutionalized
elderly subjects: a controlled trial.
Girodon F, Lombard M, Galan P, Brunet-Lecomte P, Monget AL, Arnaud J,
Preziosi P, Hercberg S.
Institut Scientifique et Technique de la Nutrition et de l'Alimentation,
Paris, France.
Ann Nutr Metab. 1997;41(2):98-107.
To determine the impact of a trace element and vitamin supplementation
on infectious morbidity, a double-blind controlled trial was performed
on 81 elderly subjects in a geriatric center during a 2-year period. Subjects
were randomly assigned to one of four treatment groups, and received daily:
placebo; trace elements/zinc 20 mg; selenium 100 micrograms); vitamins
(vitamin C 120 mg; beta-carotene 6 mg; alpha-tocopherol 15 mg); or a combination
of trace elements and vitamins at equal doses. (1) Before supplementation,
low serum values in vitamin C, folate, zinc and selenium were observed
in more than two thirds of the patients. (2) After 6 months of supplementation,
a significant increase in vitamin and trace element serum levels was obtained
in the corresponding treatment groups: a plateau was then observed for
the whole study. (3) Subjects who received trace elements (zinc and selenium)
alone or associated with vitamins had significantly less infectious events
during the 2 years of supplementation. These results indicate that supplementation
with low doses of vitamins and trace elements is able to rapidly correct
corresponding deficiencies in the institutionalized elderly. Moreover,
zinc and selenium reduced infectious events.
40. [Zinc status evaluation in an elderly institutionalized population]
[Article in Spanish]
Meertens L, Solano L, Pena E.
Unidad de Investigaciones en Nutricion, Facultad de Ciencias de la Salud,
Universidad de Carabobo, Valencia, Venezuela.
Arch Latinoam Nutr. 1997 Dec;47(4):311-4.
Elderly people is at high nutritional risk for zinc, specially marginal
deficit,
which could contribute to complications of chronic diseases and undernutrition.
The aim of study was to know the zinc status of 83 elderly people (older
than
60), from both sexes, living in geriatric home. Zinc serum levels, alkaline
phosphatase serum levels; albumin serum levels, energy, proteins and zinc
dietary intake and gustative sensitivity were determined. Results expressed
as
mean +/- DS are the following: serum zinc: 90.89 +/- 19.0 micrograms/dl,
alkaline phosphatase: 125.41 +/- 24.2 IU/L, albumin serum: 3.9 +/- 0.76
g/dl
energy intake: 1643 +/- 309.9 Kcal/day, protein intake: 59.96 +/- 13.2
g/day,
zinc intake 7.9 +/- 3.0 mg/day, only energy and zinc intake were deficient.
18.1% had zinc values under 70 micrograms/dl. There was 54% of positive
responses to the taste acuity tests. This results qualify this group as
at risk,
specially for zinc nutritional.
41. Beneficial effects of oral zinc supplementation on the immune response
of old people.
Duchateau J, Delepesse G, Vrijens R, Collet H
Am J Med 1981 May;70(5):1001-4
Zinc is known to have beneficial effects on the immune response. In an
attempt
to modify age-associated immune dysfunction, supplemental zinc was administered
to 15 subjects over 70 years of age (220 mg zinc sulfate twice daily for
a month). As compared to 15 controls, matched for age and sex, there was
a
significant improvement in the following immune parameters in the treated
group:
(1) number of circulating T lymphocytes; (2) delayed cutaneous hypersensitivity
reactions to purified protein derivative, Candidin and streptokinase-streptodornase;
(3) immunoglobulin G (IgG) antibody response to tetanus vaccine. Zinc
treatment had no influence on the number of total circulating leukocytes
or lymphocytes, or on the in vitro lymphocyte response to
three mitogens: phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed
mitogen (PWM). The data suggest that the addition of zinc to the diet
of old persons could be an effective and simple way to improve their immune
function.
42. Effect of a two-year supplementation with low doses of antioxidant
vitamins and/or minerals in elderly subjects on levels of nutrients and
antioxidant defense parameters.
Girodon F, Blache D, Monget AL, Lombart M, Brunet-Lecompte P, Arnaud
J, Richard MJ, Galan P Laboratoire de Biochimie des Lipoproteines, Universite
de Bourgogne, Digon, France.
J Am Coll Nutr 1997 Aug;16(4):357-65
BACKGROUND: Eighty-one elderly hospitalized subjects (> 65 years)
were recruited for a double-blind placebo-controlled study to examine
low dose supplementation of antioxidant vitamins and minerals on biological
and functional parameters of free radical metabolism. Subjects were randomly
assigned to one of the four treatment groups, daily receiving for 2 years:
placebo group; mineral group: 20 mg zinc, 100 micrograms selenium; vitamin
group: 120 mg VITAMIN C (Vit C), 6 mg beta-carotene (beta CA), 15 mg vitamin
E (Vit E); mineral and vitamin group: Zn 20 mg, Se 100 micrograms, Vit
C 120 mg, beta CA 6 mg, Vit E 15 mg. RESULTS: Fifty-seven subjects completed
the study. A large frequency of Vit C, Zn and Se deficiencies were observed
at baseline. As early as 6 months of treatment, a significant increase
in vitamin and mineral serum levels was observed in the corresponding
groups. The increases ranged from 1.1-4.0 fold depending on the nutrient.
Antioxidant defense, studied in vitro with a test using red blood cells
in presence of 2,2'-azo-bis (2-amidinopropane) by hydrochloride, showed
an increase of cell resistance in patients receiving vitamins (p = 0.002);
it was positively correlated with serum Vit C (p < 0.0001), alpha-tocopherol/cholesterol
(p = 0.06), beta CA (p = 0.0014), serum Cu and Se (p < 0.05). Moreover,
red blood cell antioxidant defense was reduced in elderly compared with
young control subjects (50% hemolysis time: 69 +/- 14 mn and 109 +/- 12
mn, respectively). Erythrocyte glutathione peroxidase activity was enhanced
in groups receiving minerals, whereas no significant change was observed
for other indicators of oxidative stress (erythrocyte superoxide dismutase
activity, thiobarbituric acid-reactive substances, total glutathione,
reduced and oxidized forms). DISCUSSION: Our results provide experimental
evidence that a low dose supplementation with vitamins and minerals was
able to normalize biological nutrient status as early as 6 months of treatment.
In addition, our data indicate that antioxidant defense in elderly subjects
was improved with low doses of Vit C, vit E and beta CA as studied by
means of a functional test utilizing red blood cells challenged in vitro
with free radicals.
43. In vitro modulation of keratinocyte wound healing integrins by zinc,
copper and manganese.
Tenaud I, Sainte-Marie I, Jumbou O, Litoux P, Dreno B. Laboratory of
Immuno-Dermatology, CHU Hotel-Dieu, Place A. Ricordeau, 44035 Nantes Cedex
01, France.
Br J Dermatol 1999 Jan;140(1):26-34
Although the trace elements zinc, copper and manganese are used in vivo
for their healing properties, their mechanism of action is still only
partially known. Some integrins expressed by basal layer keratinocytes
play an essential part in healing, notably alpha2beta1, alpha3beta1, alpha6beta4
and alphaVbeta5, whose expression and distribution in epidermis are modified
during the re-epithelialization phase. This study demonstrates how the
expression of these integrins are modulated in vitro by trace elements.
Integrin expression was studied in proliferating keratinocytes in monolayer
cultures and in reconstituted skin that included a differentiation state.
After 48 h incubation with zinc gluconate (0.9, 1.8 and 3.6 microg/mL),
copper gluconate (1, 2 and 4 microg/mL), manganese gluconate (0.5, 1 and
2 microg/mL) and control medium, integrin expression was evaluated by
FACScan and immunohistochemistry. Induction of alpha2, alpha3, alphaV
and alpha6 was produced by zinc gluconate 1.8 microg/mL in monolayers,
of alpha2, alpha6 and beta1 by copper gluconate 2 and 4 microg/mL and
of all the integrins studied except alpha3 by manganese gluconate 1 microg/mL.
Thus, alpha6 expression was induced by all three trace elements. The inductive
effect of zinc was particularly notable on integrins affecting cellular
mobility in the proliferation phase of wound healing (alpha3, alpha6,
alphaV) and that of copper on integrins expressed by suprabasally differentiated
keratinocytes during the final healing phase (alpha2, beta1 and alpha6),
while manganese had a mixed effect.
44. Prevalence of magnesium and zinc deficiencies in nursing home residents
in Germany.
Worwag M, Classen HG, Schumacher E. Department of Pharmacology and Toxicology
of Nutrition, University of Hohenheim, Stuttgart, Germany.
Magnes Res. 1999 Sep;12(3):181-9.
In a multicentric study with 345 seniors over 70 years old we investigated
magnesium and zinc levels in serum together with the prevalence of their
typical symptoms of deficiency in nursing home residents (NHR) and non-nursing
home residents (nNHR). In addition calcium, sodium and potassium levels
in serum were determined as well as creatinine and albumin. Considering
all seniors 33 per cent exhibited hypomagnesemia and 19 per cent hypozincemia.
Zinc levels of female and male NHR were significantly lower than levels
of nNHR. Hypomagnesemia was significantly associated with calf cramps
and with diabetes mellitus. Hypozincemia was significantly associated
with impaired wound healing.
Hearing
45. [The serum zinc level in patients with tinnitus and the effect of
zinc treatment] [Article in Japanese]
Ochi K, Ohashi T, Kinoshita H, Akagi M, Kikuchi H, Mitsui M, Kaneko T,
Kato I. Department of Otorhinolaryngology, St. Marianna University School
of Medicine, Kyoto-fu.
Nippon Jibiinkoka Gakkai Kaiho 1997 Sep;100(9):915-9
We measured the serum zinc level in patients with tinnitus and evaluated
the effectiveness of zinc in the treatment of tinnitus. Blood zinc levels
were measured in 121 patients with tinnitus. All patients were examined
between 1995 and 1997 at the outpatient clinic of otorhinolaryngology
St. Marianna University Toyoko Hospital. Forty-seven patients who had
received any drug such as a calcium channel blocker and others or had
been affected by any diseases were excluded and therefore 74 patients
consisting of 46 females (62%) and 28 males (38%) were investigated. Twenty
two healthy volunteers served as a control group. The mean age and standard
deviations for the tinnitus group and the control group were 47.8 +/-
17.1 and 31.4 +/- 8.2 years, respectively. There was a significant decrease
(p < 0.0001) in serum zinc levels in patients with tinnitus compared
with the control group. Because there was a significant difference (p
< 0.0001) in age distribution between tinnitus and control groups,
patients were selected by their age in order to neglect the effect of
aging. In this situation, a significant difference (p < 0.01) was noted
between the tinnitus group and control group. Low blood zinc level was
defined by using the mean and standard deviation for the control group
(mean-1 S.D.). We treated patients with low blood zinc levels. A total
dose of 34-68 mg of Zn++ was administered daily for over 2 weeks. The
degree of tinnitus was expressed on a numeric scale from 0 to 10 before
and after treatment. Blood zinc levels were significantly elevated (p
< 0.05) after treatment. We found a significant decrease (p < 0.01)
in the numeric scale. These findings suggest that zinc is useful in at
least some patients suffering from tinnitus. It is possible to classify
patients with tinnitus by measuring serum zinc level and this leads to
improvement of the overall treatment effect.
46. Chemical anatomy of excitatory endings in the dorsal cochlear nucleus
of the rat: differential synaptic distribution of aspartate aminotransferase,
glutamate, and vesicular zinc.
Rubio ME, Juiz JM.
Instituto de Neurociencias, Universidad Miguel Hernandez, Alicante, Spain.
lrubio@pop.nidcd.nih.gov
J Comp Neurol 1998 Sep 28;399(3):341-58
In order to identify cytochemical traits relevant to understanding excitatory
neurotransmission in brainstem auditory nuclei, we have analyzed in the
dorsal cochlear nucleus the synaptic distribution of aspartate aminotransferase,
glutamate, and vesicular zinc, three molecules probably involved in different
steps of excitatory glutamatergic signaling. High levels of glutamate
immunolabeling were found in three classes of synaptic endings in the
dorsal cochlear nucleus, as determined by quantitation of immunogold labeling.
The first type included auditory nerve endings, the second were granule
cell endings in the molecular layer, and the third very large endings,
better described as "mossy." This finding points to a neurotransmitter
role for glutamate in at least three synaptic populations in the dorsal
cochlear nucleus. The same three types of endings enriched in glutamate
immunoreactivity also contained histochemically detectable levels of aspartate
aminotransferase activity, suggesting that this enzyme may be involved
in the synaptic handling of glutamate in excitatory endings in the dorsal
cochlear nucleus. There was also extrasynaptic localization of the enzyme.
Zinc ions were localized exclusively in granule cell endings, as determined
by a Danscher-selenite method, suggesting that this ion is involved in
the operation of granule cell synapses in the dorsal cochlear nucleus.
47. The role of zinc in the treatment of tinnitus.
Arda HN, Tuncel U, Akdogan O, Ozluoglu LN.
Department of Ear, Nose, Throat, Head and Neck Surgery, Ankara Numune
Research and Education Hospital, Turkey. nedard@yahoo.com
Otol Neurotol. 2003 Jan;24(1):86-9.
OBJECTIVE: This study was designed to investigate the role of zinc
administration in treatment of tinnitus.
STUDY DESIGN: Randomized, prospective, placebo-controlled study.
SETTING: Patients with tinnitus were admitted to the ear, nose, and throat
clinic of the authors' hospital.
PATIENTS: Patients with tinnitus with no know pathologic conditions of
the ear, nose, and throat; the mean age of 28 patients receiving zinc
was 51.2 years, and that of 13 patients given placebo was 55 years.
INTERVENTION: Blood zinc levels were measured. Frequency was detected
by audiometry, and loudness of tinnitus was screened by tinnitus match
test. A questionnaire that scored tinnitus subjectively between 0 and
7 was given to patients before zinc treatment. After 2 months of treatment
(zinc 50 mg daily to zinc group, placebo pill containing starch to placebo
group), all of the tests were performed again. There was no difference
in age, sex, duration of tinnitus, and affected ears between the patients
treated with zinc and those treated with placebo. Blood zinc levels were
lower than normal in 31% of patients before treatment.
MAIN OUTCOME MEASURES: A decrease in tinnitus loudness by at least 10
dB was accepted as clinically favorable progress. A decrease of more than
1 point in subjective tinnitus scoring was accepted as valid.
RESULTS: Clinically favorable progress was detected in 46.4% of patients
given zinc. Although this decrease was not statistically significant,
the severity of subjective tinnitus decreased in 82% of the patients receiving
zinc. The mean of subjective tinnitus decreased from 5.25 +/- 1.08 to
2.82 +/- 1.81 (< 0.001). However, the decrease in severity of the tinnitus
was not significant in patients receiving placebo.
CONCLUSION: It can be concluded that patients with tinnitus may have
low blood zinc levels (31%) and clinical and subjective improvement can
be achieved by oral zinc medication. However, it remains to be seen whether
the longer duration of treatment has more significant results.
48. The role of zinc in management of tinnitus.
Yetiser S, Tosun F, Satar B, Arslanhan M, Akcam T, Ozkaptan Y.
Department of ORL and HNS, Gulhane Medical School, Etlik, 06018 Ankara,
Turkey. syetiser@yahoo.com
Auris Nasus Larynx. 2002 Oct;29(4):329-33.
OBJECTIVE: Several therapeutic modalities have been tried in patients
with
tinnitus. These trials have given rise to unsatisfactory results in most
of the
patients since the etiology and pathophysiology of tinnitus is unclear.
Significant correlation between tinnitus and decreased zinc level and
also
reduction in severity of tinnitus after zinc therapy has been reported
in some
clinical studies. The aim of this study is to find out the prevalence
of
hypozincemia in patients suffering from tinnitus of various origins
(presbyacusis, acoustic trauma and ototoxicity) at young and elderly population
and to investigate the effect of zinc therapy upon the severity of tinnitus.
METHODS: Forty consecutive patients with severe tinnitus were included
in this
study between April 1998 and May 2000. There were 32 men (80%) and eight
women (20%) with an age ranging between 19 and 67 (mean 40.6 years). Eleven
patients were over the age of 50. The zinc level was measured in non-diluted
serum by flame atomic absorption spectrophotometry (normal values; 50-120
microg/dl) from fasting blood samples. All the patients were given zinc
pills 220 mg each, once a day and 2 h before lunch for 2 months. The patients
were required to fulfill a tinnitus scoring scale and a handicap questionnaire
before and after treatment. The Wilcoxon rank sum test and McNemar test
were used for the statistical analysis.
RESULTS: Six patients were hypozincemic and seven patients had decreased
serum zinc levels. No significant change has been observed in frequency
and severity of tinnitus measured by audiologic tests after zinc therapy.
Twenty-three (57.5%) of these patients reported some relief of tinnitus
in the tinnitus scoring scale but the rate of improvement was minor (P>0.05).
Decrease in severity of tinnitus after zinc therapy in elder group was
better than the younger ones.
CONCLUSION: Our study could not confirm the high incidence of hypozincemia
in patients with tinnitus as reported previously. Zinc therapy for 8 weeks
presented no promising effect on tinnitus in three groups of patients
and the difference between the rate of improvement in severity of tinnitus
after zinc intake in patients with normal and low serum zinc level was
not significant. Zinc supplement provided relief of tinnitus in some of
the elder people who apparently had dietary zinc deficiency.
49. Zinc: the neglected nutrient.
Shambaugh GE Jr.
Shambaugh Hearing and Allergy, Hinsdale, IL 60521.
Am J Otol 1989 Mar;10(2):156-60
Zinc was first recognized as essential for animals at the University
of Illinois School of Agriculture in 1916, when it was found that zinc-deficient
baby pigs were runty, developed dermatitis on their legs, and were sterile.
Zinc deficiency was first recognized in man by Dr. Ananda Prasad of Detroit
26 years ago when he measured serum and hair zinc levels in young male
Egyptian dwarfs who had failed to mature and were small in stature. By
simply adding zinc to their regular diet, they grew in height and became
sexually mature. It is now recognized that dwarfism in males is frequent
around the Mediterranean, where wheat is the staple of life and has been
grown for 4,000 years on the same soil, thereby resulting in the depletion
of zinc. Professor Robert Henkin first suggested that zinc deficiency
might cause hearing-nerve impairment. Assay of the soft tissues of the
cochlea and vestibule revealed a zinc level higher than that of any other
part of the body. Previously, the eye was considered to have the highest
level of zinc of any organ. To diagnose zinc deficiency clinically, we
use serum zinc assays made at the Mayo Clinic Trace Element Laboratory.
With zinc supplementation in patients who are marginally zinc deficient,
there has been improvement in tinnitus and sensorineural hearing loss
in about one-third of elderly adults. We believe zinc deficiency is one
causation of presbycusis; by recognizing and correcting it, a progressive
hearing loss can be arrested.
Hepatitis
50. Determination of hepatic zinc content in chronic liver disease due
to hepatitis B virus.
Gur G; Bayraktar Y; Ozer D; Ozdogan M; Kayhan B
Hacettepe University, Faculty of Medicine, Department of Internal Medicine,
Ankara-Turkey.
Hepatogastroenterology (Greece) Mar-Apr 1998, 45 (20) p472-6
BACKGROUND/AIMS: Zinc is an essential, mostly intracellular, trace element
which participates in many physiologic mechanisms. Some liver functions
like urea formation require the presence of zinc; thus the determination
of hepatic zinc content may contribute to the understanding of probable
zinc-related clinical consequences of chronic liver disease. In this study,
we aimed to determine the hepatic zinc concentrations in patients with
chronic liver disease due to the Hepatitis B virus and to ascertain the
relationship between the severity of liver disease and hepatic zinc content,
if one in fact exists.
METHODOLOGY: A total of 99 HBsAg positive subjects were included in the
study. We performed a liver biopsy on all subjects. Hepatic zinc concentrations
were determined by atomic absorption spectrophotometry.
RESULTS: The liver biopsies were normal in 25 subjects. There were 33
chronic active hepatitis (CAH), 34 cirrhosis and 7 chronic persistent
hepatitis (CPH) patients in the study group. In the control group, CAH,
cirrhosis and CPH groups, the mean liver zinc concentrations were 3.83
+/- 1.86, 1.86 +/- 0.92, 1.14 +/- 0.68 and 3.74 +/- 1.81 mumol/g dry weight,
respectively. Hepatic zinc in the CAH and cirrhosis groups were lower
than that of the control group (p < 0.05). We also found that liver
zinc in the cirrhosis group was lower than in the CAH group (p < 0.05).
CONCLUSION: According to these results, as the severity of liver damage
increases, the hepatic zinc concentration decreases. Therefore, it can
be suggested that zinc supplementation may improve hepatic encephalopathy
by increasing the efficiency of the urea cycle.
51. Zinc supplementation improves glucose disposal in patients with cirrhosis.
Marchesini G; Bugianesi E; Ronchi M; Flamia R; Thomaseth K; Pacini G
Dipartimento di Medicina Interna, Cardioangiologia, Epatologia, Universita
di Bologna, Italy.
Metabolism (United States) Jul 1998, 47 (7) p792-8
Zinc deficiency is common in cirrhosis, and was proved to affect nitrogen
metabolism. In experimental animals, zinc status may also affect glucose
disposal, and acute zinc supplementation improves glucose tolerance in
healthy subjects. This study was aimed at measuring the effects of long-term
oral zinc supplements on glucose tolerance in cirrhosis . The time courses
of glucose, insulin, and C-peptide in response to an intravenous (i.v.)
glucose load were analyzed by the minimal-model technique before and after
long-term oral zinc supplements (200 mg three times per day for 60 days)
in 10 subjects with advanced cirrhosis and impaired glucose tolerance
or diabetes. The test was performed using a simplified procedure, based
on 20 blood samples collected within 4 hours from the glucose load. Normal
values were obtained in 25 age-matched healthy subjects. Zinc levels were
low to normal or reduced before treatment, and were normalized by oral
zinc. Glucose disappearance improved by greater than 30% in response to
treatment. There were no changes in pancreatic insulin secretion and systemic
delivery, or in the hepatic extraction of insulin. Insulin sensitivity
(SI), which was reduced by 80% before treatment, did not change. Glucose
effectiveness (SG) was nearly halved in cirrhosis before treatment (0.013
[SD 0.007] min(-1) v. 0.028 [SD 0.009] in controls; P < .001), and
increased to 0.017 (SD 0.009) after zinc (P < .05 v. baseline). The
return to normal of plasma zinc levels after long-term zinc treatment
in advanced cirrhosis improves glucose tolerance via an increase of the
effects of glucose per se on glucose metabolism. Poor zinc status may
contribute to the impaired glucose tolerance and diabetes of cirrhosis.
52. Effect of dietary zinc deficiency on alkaline phosphatase and nucleic
acids in rats.
Okegbile EO, Odunuga O, Oyewo A. Department of Biochemistry, Ogun State
University, Ago-Iwoye, Nigeria.
Afr J Med Med Sci. 1998 Sep-Dec;27(3-4):189-92
Weanling male albino rats were randomly alloted to zinc deficient fed
(ZnDF) pair-fed (ZnPF) or ad libitum-fed (ZnAL) dietary treatments. The
rats were fed diets with either low (5 micrograms/g) or adequate (100
micrograms/g) zinc for 28 days. Zinc deficiency significantly reduced
growth rate by 60% and was associated with a significantly low feed intake
when compared with ZnPF and ZnAL groups. DNA and RNA contents of the liver
were used as indication of nitrogen metabolism. DNA content was similar
for both ZnPF and ZnAL groups (1.90 and 2.20 mg/g wet weight, respectively),
but significantly different from ZnDF (1.42 mg/g wet weight). Liver RNA
values of ZnAL, ZnPF and ZnDF groups similarly varied (25.0, 20.2 and
14.8 mg/g wet weight, respectively). Liver, muscle, spleen, femur and
serum zinc concentrations were lowest in rats fed ZnDF relative to adequate
zinc levels. The levels of the alkaline phosphatase activity was highest
in the serum and lowest in the brain (spleen value was greater than that
of the liver). Alkaline phosphatase activity was similar in ZnAL and ZnPF
groups, but significantly different from ZnDF. In conclusion, the constitutively
expressed growth rate, DNA level, RNA level, organ/serum zinc contents
and alkaline phosphatase activities were markedly affected by zinc deficiency
in rats.
HIV
53. Zinc status in human immunodeficiency virus type 1 infection and
illicit drug use.
Baum MK, Campa A, Lai S, Lai H, Page JB.
Florida International University, College of Health and Urban Affairs,
University Park, Rm. HLS 337, Miami, FL 33199, USA. baumm@fiu.edu
Clin Infect Dis. 2003;37 Suppl 2:S117-23.
Zinc deficiency is the most prevalent micronutrient abnormality seen
in human
immunodeficiency virus (HIV) infection. Low levels of plasma zinc predict
a
3-fold increase in HIV-related mortality, whereas normalization has been
associated with significantly slower disease progression and a decrease
in the
rate of opportunistic infections. Studies in Miami, Florida, indicated
that
HIV-positive users of illicit drugs are at risk for developing zinc deficiency,
at least partially because of their poor dietary intake. Zinc deficiency
characterized by low plasma zinc levels over time enhances HIV-associated
disease progression, and low dietary zinc intake is an independent predictor
of
mortality in HIV-infected drug users. The amount of zinc supplementation
in HIV
infection appears to be critical, because deficiency, as well as excessive
dietary intake of zinc, has been linked with declining CD4 cell counts
and
reduced survival. More research is needed to determine the optimal zinc
supplementation level in HIV-infected patients, to prevent further burden
on an
already compromised immune system.
54. Modulatory effects of selenium and zinc on the immune system.
Ferencik M, Ebringer L.
Institute of Immunology, Faculty of Medicine, Comenius University, Institute
of
Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovakia.
Folia Microbiol (Praha). 2003;48(3):417-26.
Almost all nutrients in the diet play a crucial role in maintaining an
"optimal"
immune response, and both insufficient and excessive intakes can have
negative
consequences on the immune status and susceptibility to a variety of pathogens.
We summarize the evidence for the importance of two micronutrients, selenium
and zinc, and describe the mechanisms through which they affect the immune
status and other physiological functions. As a constituent of selenoproteins,
selenium is needed for the proper functioning of neutrophils, macrophages,
NK cells, T lymphocytes and some other immune mechanisms. Elevated selenium
intake may be associated with reduced cancer risk and may alleviate other
pathological conditions including oxidative stress and inflammation. Selenium
appears to be a key nutrient in counteracting the development of virulence
and inhibiting HIV progression to AIDS. It is required for sperm motility
and may reduce the risk of miscarriage. Selenium deficiency has been linked
to adverse mood states and some findings suggest that selenium deficiency
may be a risk factor in cardiovascular diseases. Zinc is required as a
catalytic, structural and
regulatory ion for enzymes, proteins and transcription factors, and is
thus a
key trace element in many homeostatic mechanisms of the body, including
immune responses. Low zinc ion bioavailability results in limited immunoresistance
to infection in aging. Physiological supplementation of zinc for 1-2 months
restores immune responses, reduces the incidence of infections and prolongs
survival. However, in every single individual zinc supplementation of
food should be adjusted to the particular zinc status in views of the
great
variability in habitat conditions, health status and dietary requirements.
55. Nutrients and HIV: part two-vitamins A and E, zinc, B-vitamins, and
magnesium.
Patrick L.
Altern Med Rev 2000 Feb;5(1):39-51
There is compelling evidence that micronutrient deficiencies can profoundly
affect immunity; micronutrient deficiencies are widely seen in HIV, even
in asymptomatic patients. Direct relationships have been found between
deficiencies of specific nutrients, such as vitamins A and B12, and a
decline in CD4 counts. Deficiencies appear to influence vertical transmission
(vitamin A) and may affect progression to AIDS (vitamin A, B12, zinc).
Correction of deficiencies has been shown to affect symptoms and disease
manifestation (AIDS dementia complex and B12; diarrhea, weight loss, and
zinc), and certain micronutrients have demonstrated a direct anti-viral
effect in vitro (vitamin E and zinc). The previous article in this series
focused on selenium and beta carotene deficiencies in HIV/AIDS. This literature
review elucidates how deficiencies of the micronutrients zinc, magnesium,
vitamins A, E, and specific B vitamins relate to HIV symptomology and
progression, and clearly illustrates the need for nutritional supplementation
in HIV disease.
56. Zinc serum level in human immunodeficiency virus-infected patients
in relation to immunological status.
Wellinghausen N, Kern WV, Jochle W, Kern P. Section of Infectious Diseases
and Clinical Immunology, Medical University of Ulm, Germany.
Biol Trace Elem Res 2000 Feb;73(2):139-49
In human immunodeficiency virus (HIV) infection, serum level of zinc,
an important micronutrient for immune function, is frequently diminished.
The aim of this study was to determine the zinc status in relation to
immunological parameters and disease stage in 79 HIV-1 seropositive patients.
The median serum level of zinc was within normal limits (12.5 micromol/L)
but in 23% of patients, zinc deficiency was seen. Decreased serum zinc
was associated with a low CD4 cell count, high viral load, and increased
neopterin and IgA levels. According to current treatment recommendations,
the majority of patients received antiretroviral triple therapy. Zinc
levels in treated and untreated patients were comparable. Referring to
disease stage (CDC classification, 1993), the mean zinc level was highest
in stage C and lowest in stage A. In conclusion, even under antiretroviral
triple therapy, zinc deficiency is still of great importance in HIV infection,
and zinc substitution in zinc deficient individuals should be taken into
account to optimize therapeutical success.
57. Zinc serum level in human immunodeficiency virus-infected patients
in relation to immunological status.
Wellinghausen N, Kern WV, Jochle W, Kern P.
Section of Infectious Diseases and Clinical Immunology, Medical University
of
Ulm, Germany.
Biol Trace Elem Res. 2000 Feb;73(2):139-49.
In human immunodeficiency virus (HIV) infection, serum level of zinc,
an
important micronutrient for immune function, is frequently diminished.
The aim
of this study was to determine the zinc status in relation to immunological
parameters and disease stage in 79 HIV-1 seropositive patients. The median
serum level of zinc was within normal limits (12.5 micromol/L) but in
23% of patients, zinc deficiency was seen. Decreased serum zinc was associated
with a low CD4 cell count, high viral load, and increased neopterin and
IgA levels. According to current treatment recommendations, the majority
of patients received antiretroviral triple therapy. Zinc levels in treated
and untreated patients
were comparable. Referring to disease stage (CDC classification, 1993),
the mean zinc level was highest in stage C and lowest in stage A. In conclusion,
even under antiretroviral triple therapy, zinc deficiency is still of
great
importance in HIV infection, and zinc substitution in zinc deficient individuals
should be taken into account to optimize therapeutical success.
Hypertension
58. Free radical disease prevention and nutrition.
Krajcovicova-Kudlackova M, Ursinyova M, Blazicek P, Spustova V, Ginter
E,
Hladikova V, Klvanova J.
Institute of Preventive and Clinical Medicine, Bratislava, Slovakia.
Kudlackova@upkm.sk
Bratisl Lek Listy. 2003;104(2):64-8.
An improved antioxidant status (overthreshold plasma values of essential
antioxidants) minimizes the oxidative damage. The levels of antioxidant
vitamins
C and E, ,,antioxidant" trace elements selenium, zinc, copper and
iron were
measured in two groups of adults with different nutritional habits--alternative
(vegetarians; n=110) and traditional (mixed diet, control, n=101). The
prevalence of iron and zinc deficiencies was found in the alternative
group (20%
vs 11%--iron, 13% vs 9%--zinc) as a consequence of higher intake of plant
trace
element absorption inhibitors. As opposed to the latter, the control group
had
higher findings of iron and copper levels over the optimal range (18%
vs
8%--iron, 11% vs 2%--copper). The subjects on mixed diet was showed a
significant negative linear correlation between serum zinc and iron levels.
This
favourable relationship means a decrease in Fenton reaction by indirect
zinc
effect. Average plasma values of vitamin C, vitamin C/vitamin E, vitamin
E/
cholesterol (LDL protection), vitamin E/triacylglycerols (polyunsaturated
fatty
acid protection) in vegetarians are over the threshold with high number
of
individual overthreshold values (94% vs 17%--vitamin C, 100% vs 58%--vitamin
C/vitamin E, 89% vs 68%--vitamin E/cholesterol, 100% vs 64%--vitamin
E/triacylglycerols). Homocysteine levels in vegetarians (36% atherogenic
levels)
correlate significantly inversely to vitamin C levels, the fact of which
means a
positive vitamin C effect in free radical remove also in hyperhomocysteinemia.
Plant food is a rich source of antioxidants. A correct vegetarian nutrition
or
optimized mixed diets with regular and frequent consumption of protective
food
commodities may be an effective contribution to the age-related chronic
degenerative disease prevention. (Tab. 2, Fig. 2, Ref. 31.).
59. Angiotensin-I-converting enzyme and its relatives.
Riordan JF.
Center for Biochemical and Biophysical Sciences and Medicine, Harvard
Medical
School, One Kendall Square, Cambridge, MA 02139, USA.
james_riordan@hms.harvard.edu
Genome Biol. 2003;4(8):225. Epub 2003 Jul 25.
SUMMARY: Angiotensin-I-converting enzyme (ACE) is a monomeric, membrane-bound,
zinc- and chloride-dependent peptidyl dipeptidase that catalyzes the conversion
of the decapeptide angiotensin I to the octapeptide angiotensin II, by
removing a carboxy-terminal dipeptide. ACE has long been known to be a
key part of the renin angiotensin system that regulates blood pressure,
and ACE inhibitors are important for the treatment of hypertension. There
are two forms of the enzyme in humans, the ubiquitous somatic ACE and
the sperm-specific germinal ACE, both encoded by the same gene through
transcription from alternative promoters. Somatic ACE has two tandem active
sites with distinct catalytic properties, whereas germinal ACE, the function
of which is largely unknown, has just a single active site. Recently,
an ACE homolog, ACE2, has been identified in humans that differs from
ACE in being a carboxypeptidase that preferentially removes carboxy-terminal
hydrophobic or basic amino acids; it appears to be important in cardiac
function. ACE homologs (also known as members of the M2 gluzincin family)
have been found in a wide variety of species, even in those that neither
have a cardiovascular system nor synthesize angiotensin. X-ray structures
of a truncated, deglycosylated form of germinal ACE and a related enzyme
from Drosophila have been reported, and these show that the active site
is deep within a central cavity. Structure-based drug design targeting
the individual active sites of somatic ACE may lead to a new generation
of ACE inhibitors, with fewer side-effects than currently available inhibitors.
60. Studies of five microelement contents in human serum, hair, and fingernails
correlated with aged hypertension and coronary heart disease.
Tang YR, Zhang SQ, Xiong Y, Zhao Y, Fu H, Zhang HP, Xiong KM.
College of Chemistry and Molecular Science, College of Life Sciences,
Wuhan
University, 430072 Wuhan Hubei, China.
Biol Trace Elem Res. 2003 May;92(2):97-104.
Using atomic absorption spectrometry (AAS), five microelements in human
serum, hair, and fingernails of aged hypertension, coronary heart disease
(diseased group) and aged health control (healthy group) were detected.
Results of the t-test are as follows: The iron, zinc, and cadmium contents
and Zn/Cu (mol/mol) ratio of the diseased group were significantly higher
than that of the healthy group in serum (p<0.01, p<0.05, p<0.01,
and p<0.05, respectively); the chromium contents in the serum, hair,
and fingernails (p<0.05, p<0.01, and p<0.05, respectively); the
iron and zinc contents in the hair and fingernails (p<0.01, p<0.001,
p<0.05, and p<0.01 respectively) and Zn/Cu ratio in the hair (p<0.01)
of the diseased group were significantly lower than that of the healthy
group.
61. Zn deficiency aggravates hypertension in spontaneously hypertensive
rats:
possible role of Cu/Zn-superoxide dismutase.
Sato M, Yanagisawa H, Nojima Y, Tamura J, Wada O.
Department of Hygiene and Preventive Medicine, Faculty of Medicine, Saitama
Medical School, Iruma-gun, Japan.
Clin Exp Hypertens. 2002 Jul;24(5):355-70.
Using spontaneously hypertensive rats (SHR) fed a standard or a Zn-deficient
diet for 4 weeks, we examined whether Zn deficiency affects systemic blood
pressure (BP) levels in a genetically hypertensive state through a fall
in the
activity of Cu/Zn-superoxide dismutase (SOD). SHR fed a Zn-deficient diet
had a
progressive increase in systolic BP during the dietary conditioning.
Consequently, SHR fed a Zn-deficient diet exhibited significantly increased
levels of systolic BP by 2 weeks after the start of dietary treatment
when
compared with SHR fed a standard diet. Similarly, levels of basal mean
arterial
pressure (MAP) observed at the end of dietary treatment were SHR fed a
Zn-deficient diet > SHR fed a standard diet. Administration of the
nitric oxide
synthase (NOS) inhibitor, L-NAME, caused an increase in MAP levels in
the two
groups of rats, demonstrating the involvement of the vasodilator, nitric
oxide
(NO), in the regulation of systemic BP in a genetically hypertensive state.
The
expression of endothelial (e) NOS mRNA and protein in the thoracic aorta
paralleled basal MAP levels in the two groups of rats, suggesting the
counter-regulation of eNOS against the developed hypertensive state in
SHR fed a Zn-deficient diet. On the other hand, administration of the
superoxide
scavenger, tempol (a SOD mimetic compound), led to a decrease in MAP levels
in the two groups of rats, indicating the participation of the oxygen
free radical,
superoxide, in an increase in systemic BP in a genetically hypertensive
state.
As reported recently, the mechanism involved is due likely to a decrease
in the
action of the vasodilator, NO, based on the formation of peroxynitrite
coming
from the non-enzymatic reaction of superoxide and NO. In addition, tempol
treatment completely restored MAP levels in SHR fed a Zn-deficient diet
to
levels comparable to those observed in SHR fed a standard diet, indicating
that
a further increase in systemic BP levels seen in SHR fed a Zn-deficient
vs. a
standard diet is presumably brought by a reduction in the action of the
vasodilator, NO, resulting from an increase in the action of superoxide.
The
activity of the superoxide scavenger, Cu/Zn-SOD, in the thoracic aorta
was
significantly decreased in SHR fed a Zn-deficient diet relative to SHR
fed a
standard diet. It appears that a decrease in the activity of Cu/Zn-SOD
observed
in the thoracic aorta of SHR fed a Zn-deficient diet at least in part
plays a
role in an increase in the action of superoxide in this model. Thus, Zn
deficiency may be a factor to develop genetic hypertension presumably
through
the oxidative stress caused by superoxide.
62. Increased absorption of zinc from alimentary tract in primary arterial
hypertension.
Tubek S.
Department of Internal Diseases, Regional Hospital, Strzelce Opolskie,
Faculty
of Physical Education and Physiotherapy, Institute of Technology, Opole,
Poland.
szpital.strzelce-op.pl
Biol Trace Elem Res. 2001 Oct;83(1):31-8.
Zinc absorption from the alimentary tract, as revealed by serum zinc
concentration, was studied in a group of 10 patients (age 37.7+/-5.1 yr)
with
moderate and severe untreated primary arterial hypertension before and
after a
30-d treatment with perindopril 4 mg/d. Blood pressure was
177.33+/-16.24/111.33+/-15.26 mm Hg before and 143.41+/-17.34/91.29+/-12.54
mm Hg after treatment (p < 0.05/p < 0.05). Nine persons (age 37+/-6.2
yr) with
normal blood pressure (121.33+/-9.9/78+/-5.23 mm Hg) were the control
group.
Blood samples were taken from the ulnar vein at 8.00 AM (0 h), before
taking
zinc orally (one tablet of Zincas (zinc aspartate), containing 5 mg Zn2+)
and at
1, 3, and 6 h after the dose. Serum zinc concentration in control and
hypertensive group (before treatment) were initially 15.47+/-6.26 versus
15.99+/-5.65 (NS), 19.37+/-6.40 versus 20.83+/-4.48 (NS) after 1 h, 17.91+/-4.76
versus 31.32+/-10.49 (p < 0.003) after 3 h, and 15.32+/-5.47 versus
17.87+/-6.56
(NS) after 6 h. Maximal increase of Zn was 4.77+/-2.10 versus 17.53+/-4.13,
respectively (p < 0.001). In the hypertensive group, serum Zn before
and after
perindopril treatment was initially 15.98+/-5.65 versus 14.81+/-3.11 (NS),
20.83+/-4.48 versus 18.17+/-2.50 (NS) after 1 h, 31.32+/-10.49 versus
22.94+/-5.80 (NS) after 3 h, 17.53+/-4.13 (p < 0.001) after 6 h. Maximal
increase of Zn before treatment was 17.53+/-4.13 versus 9.17+/-4.67 (p
< 0.017)
after treatment. The following conclusions were reached: (1) In patients
with
primary arterial hypertension, an increased zinc absorption from alimentary
tract was found; (2) A 30-d perindopril treatment 4 mg/d orally decreased
zinc
absorption in these patients.
63. Zinc and copper status and blood pressure.
Bergomi M, Rovesti S, Vinceti M, Vivoli R, Caselgrandi E, Vivoli G.
Department of Biomedical Sciences, University of Modena, Italy.
J Trace Elem Med Biol. 1997 Nov;11(3):166-9.
Comment in:
J Trace Elem Med Biol. 1998 Mar;12(1):1.
In order to elucidate the relationships between Zn and Cu and blood pressure,
the present case-control study was carried out. Zn and Cu status was evaluated
in 60 subjects, pharmacologically untreated, affected by mild stable
hypertension and in 60 normotensives matched for sex, age and smoking
habits.
Different markers of Zn and Cu status, including serum, erythrocyte and
urine
levels of the two trace elements and activities of some Zn- or Cu-dependent
enzymes (alkaline phosphatase, lactic dehydrogenase, superoxide dismutase
and lysyl oxidase) were evaluated. No significant difference between hypertensives
and normotensives was observed in the mean levels of Zn and Cu as well
as in Zn- or Cu-dependent enzymes, though higher levels of serum copper
were associated with increased risk of hypertension. Interesting relationships
between the biological parameters investigated were observed in the hypertensive
subjects. Inverse correlations between blood pressures and serum Zn were
observed. Furthermore, blood pressure was inversely related to lysyl oxidase
activity. These findings give further support to the hypothesis that an
imbalance of Zn and Cu bioavailability may be associated to hypertensive
condition.
64. [Evaluation of selected parameters of zinc metabolism in patients
with primary hypertension]
Peczkowska M; Kabat M; Janaszek-Sitkowska H; PuLawska M
Kliniki Nadcisnienia Tetniczego Instytutu Kardiologii w Warszawie.
Pol Arch Med Wewn (Poland) Mar 1996, 95 (3) p198-204
The aim of the study was to investigate the role of zinc (Zn) in essential
hypertension (EH).
PATIENTS AND METHODS: Material of the study consisted of 31 patients
(12 female, 19 male) with mild and moderate EH and 20 healthy persons
(NT) (7 female, 13 male). Erythrocyte (ZnE) and serum (ZnS) zinc as well
as 24 hour urinary zinc excretion (ZuU) were assessed in both groups.
Zn parameters were measured by atomic absorption spectrophotomery.
RESULTS: ZnS was lower and ZnE was higher in EH (p < 0.001) than in
normotensives. ZnU did not differ between EH and NT. ZnE and ZnS negatively
correlated with age in NT but not in EH, ZnU negatively correlated with
age only in EH. BP positively correlated with ZnS in EH but not in NT.
In both groups negative correlations were found between BP and ZnU.
CONCLUSIONS: 1. Zinc probably plays a role in pathogenesis of essential
hypertension.
65. Zinc, cadmium, and hypertension in parturient women
Lazebnik N; Kuhnert BR; Kuhnert PM
Department of Obstetrics and Gynecology, Cleveland Metropolitan General
Hospital, OH 44109.
Am J Obstet Gynecol (United States) Aug 1989, 161 (2) p437-40
Zinc deficiency and cadmium toxicity have both been implicated in hypertension
during pregnancy. The goals of this study were twofold: first, to assess
the different zinc indices (plasma, red blood cell zinc, heat-labile alkaline
phosphatase, and placental zinc) in normotensive and hypertensive parturients
to determine whether they are altered in the different types of hypertension
that occur during pregnancy; second, to assess whole-blood cadmium and
placental cadmium with regard to hypertension and zinc status. Patients
were diagnosed as having chronic hypertension or preeclamptic toxemia
and were then further divided into groups on the basis of smoking status.
Each patient was matched with a normal control subject based on age, parity,
and smoking status. Forty-three hypertensive patients and their matched
control subjects were studied. No differences were found in the various
zinc indices between chronic hypertensive parturients and normal control
subjects. However, in parturients with preeclamptic toxemia, the plasma
zinc level was 19% lower than in control subjects (p less than 0.02);
these patients had the lowest plasma zinc level of the three groups. Placental
zinc was also 12% lower in patients with preeclamptic toxemia than in
control subjects (p less than 0.04). Whole-blood cadmium and placental
cadmium levels did not differ between control subjects or hypertensive
patients. However, a significant positive correlation was found between
whole-blood cadmium and plasma zinc levels in preeclamptic toxemia (r
= 0.53; p less than 0.05). The results support a marginal zinc deficiency
in parturients with preeclamptic toxemia but not in those with chronic
hypertension. The role of cadmium in the cause of preeclamptic toxemia
remains unclear.
Immune Enhancement
66. Zinc treatment prevents lipid peroxidation and increases glutathione
availability in Wilson's disease.
Farinati F, Cardin R, D'inca R, Naccarato R, Sturniolo GC.
Department of Surgical and Gastroenterological Sciences, University of
Padua,
Padua, Italy.
J Lab Clin Med. 2003 Jun;141(6):372-7.
Oxidative and reductive mechanisms are important in Wilson's disease.
In this
study, we sought to evaluate tissue levels of glutathione and cysteine,
an
important detoxification system, and of malondialdehyde, a marker of
lipoperoxidation, in patients with Wilson's disease receiving penicillamine
or
zinc treatment, in comparison with patients with chronic liver disease
of
different origin. Concentrations of cysteine, reduced/oxidized glutathione,
malondialdehyde, zinc, and copper were determined (with the use of high-pressure
liquid chromatography, fluorimetry and atomic-absorption spectrophotometry)
in liver-biopsy specimens from 24 patients with Wilson's disease (18 treated
with zinc, 6 with penicillamine), 34 patients with chronic viral hepatitis,
and 10 patients with alcoholic liver disease. In patients with Wilson's
disease, the concentration of reduced glutathione was lower than that
in patients with viral hepatitis and as high as that in subjects with
alcoholic liver damage. The cysteine level was significantly lower than
those in the control groups, and the percentage of oxidized glutathione/total
glutathione was higher than that in
viral or alcoholic disease. Malondialdehyde levels were low, but when
zinc- and
penicillamine-treated patients were considered separately, only the former
had
low malondialdehyde levels. Zinc-treated patients had higher concentrations
of
reduced glutathione and a lower percentage of oxidized glutathione. In
summary,
patients with Wilson's disease have relevant glutathione depression, with
low
levels of reduced glutathione and cysteine and high concentrations of
oxidized
glutathione: This is prevented by zinc administration, which inhibits
lipid
peroxidation and increases glutathione availability.
67. Zinc-altered immune function.
Ibs KH, Rink L.
Institute of Immunology, University Hospital, Technical University of
Aachen,
D-52074 Aachen, Germany.
J Nutr. 2003 May;133(5 Suppl 1):1452S-6S.
Zinc is known to be essential for all highly proliferating cells in the
human
body, especially the immune system. A variety of in vivo and in vitro
effects of
zinc on immune cells mainly depend on the zinc concentration. All kinds
of
immune cells show decreased function after zinc depletion. In monocytes,
all
functions are impaired, whereas in natural killer cells, cytotoxicity
is
decreased, and in neutrophil granulocytes, phagocytosis is reduced. The
normal
functions of T cells are impaired, but autoreactivity and alloreactivity
are
increased. B cells undergo apoptosis. Impaired immune functions due to
zinc
deficiency are shown to be reversed by an adequate zinc supplementation,
which
must be adapted to the actual requirements of the patient. High dosages
of zinc
evoke negative effects on immune cells and show alterations that are similar
to
those observed with zinc deficiency. Furthermore, when peripheral blood
mononuclear cells are incubated with zinc in vitro, the release of cytokines
such as interleukins (IL)-1 and -6, tumor necrosis factor-alpha, soluble
IL-2R
and interferon-gamma is induced. In a concentration of 100 micro mol/L,
zinc
suppresses natural killer cell killing and T-cell functions whereas monocytes
are activated directly, and in a concentration of 500 micro mol/L, zinc
evokes a
direct chemotactic activation of neutrophil granulocytes. All of these
effects
are discussed in this short overview.
68. Metallothioneins/PARP-1/IL-6 interplay on natural killer cell activity
in
elderly: parallelism with nonagenarians and old infected humans. Effect
of zinc supply.
Mocchegiani E, Muzzioli M, Giacconi R, Cipriano C, Gasparini N, Franceschi
C,
Gaetti R, Cavalieri E, Suzuki H.
Immunology Center (Section Nutrition, Immunity and Ageing), Research Department
Italian National Research Centres on Ageing (INRCA), Via Birarelli 8,
60121, Ancona, Italy
Mech Ageing Dev. 2003 Apr;124(4):459-68.
Metallothioneins (MTs) play pivotal role in zinc-related cell homeostasis
because of their high affinity for this trace element which is in turn
relevant
against oxidative stress and for the efficiency of the entire immune system,
including natural killer (NK) cell activity. In order to accomplish this
role,
MTs sequester and/or dispense zinc during stress and inflammation to protect
cells against reactive oxygen species. MTs gene expression is affected
by IL-6
for a prompt immune response. Concomitantly, MTs release zinc for the
activity
of antioxidant zinc-dependent enzymes, including poly(ADP-ribose)polymerase-1(PARP-1),
which is involved in base excision DNA-repair. This role of MTs is peculiar
in young adult-age during transient stress and inflammation, but not in
ageing because stress-like condition and inflammation are persistent.
This may lead MTs to turn-off from role of protection in young age to
deleterious one in ageing with subsequent appearance of age-related diseases
(severe infections). The aim is to study the role played by MTs/IL-6/PARP-1
interplay on NK cell activity in elderly, in old infected patients (acute
and remission phases by bronchopneumonia infection) and in health nonagenarian/centenarian
subjects. MTmRNA is high in lymphocytes from elderly people coupled with
high IL-6, low zinc ion bioavailability, decreased NK cell activity and
impaired capacity of PARP-1 in base excision DNA-repair. The same trend
in this altered physiological cascade during ageing also occurs in old
infected patients (both acute and remission phases) with more marked immune
damage, inflammatory condition and very impaired PARP-1 in base excision
DNA-repair. By contrast, centenarian subjects display low MTmRNA, good
zinc ion bioavailability, satisfactory NK cell activity and higher capacity
of PARP-1 in base excision DNA-repair. These findings clearly demonstrate
that the sequester of zinc by MTs in ageing is deleterious because leading
to low zinc ion bioavailability with subsequent impairment of PARP-1 and
NK cell activity and appearance of severe infections. Physiological zinc
supply (12 mg Zn(++)/day) for 1 month in elderly and in old infected patients
(remission phase) restores NK cells activity with values observed in health
centenarians. Therefore, the zinc ion bioavailability by zinc-bound MTs
homeostasis is pivotal to reach health longevity and successful ageing.
69. Zinc and immune function.
Dardenne M.
CNRS UMR 8603, Universite Paris V, Hopital Necker, Paris, France.
dardenne@necker.fr
Eur J Clin Nutr. 2002 Aug;56 Suppl 3:S20-3.
It is well recognized that zinc is an essential trace element, influencing
growth and affecting the development and integrity of the immune system.
Research has begun to clarify the molecular mechanisms underlying the
action of zinc on the immune function. It is clear that this trace element
has a broad
impact on key immunity mediators, such as enzymes, thymic peptides and
cytokines, explaining the paramount importance of zinc's status on the
regulation of lymphoid cell activation, proliferation and apoptosis. Ongoing
and
future studies regarding the immunological status of zinc deficiency 'at
risk'
groups could lead to public health interventions with nutritional doses
of zinc
supplements to prevent alteration of the immune system and improve resistance
to infections.
70. Zinc deficiency impairs immune responses against parasitic nematode
infections at intestinal and systemic sites.
Scott ME, Koski KG.
Institute of Parasitology, School of Dietetics and Human Nutrition, McGill
University, Macdonald Campus, Ste-Anne de Bellevue, Quebec H9X 3V9, Canada.
J Nutr. 2000 May;130(5S Suppl):1412S-20S.
Research on the complex interactions among host nutritional status, parasitic
infection and immune responsiveness has focused on the detrimental consequences
of parasitic infections on host nutritional status and on mechanisms by
which malnutrition impairs immunocompetence. Curiously, relatively few
studies have examined the effects of malnutrition on the immune response
in the parasite-infected host, and even fewer have considered the events
occurring at the intestinal level, where absorption of nutrients occurs,
intestinal parasites reside, and the gastrointestinal-associated lymphoid
tissues play a role in directing both the local and the more systemic
immune responses. Our work using a zinc-deficient nematode-infected mouse
model reveals that parasites are better able to survive in the zinc-deficient
hosts than in well-nourished hosts; that the production of interleukin-4
in the spleen of zinc-deficient mice is depressed, leading to depressed
levels of IgE, IgG(1) and eosinophils; and that the function of T cells
and antigen-presenting cells is impaired by zinc deficiency as well as
by energy restriction. Given the paramount role of the gastrointestinal-associated
lymphoid tissues in inducing and regulating immune responses to intestinal
parasites and in orchestrating responses in the spleen and peripheral
circulation, we conclude that zinc deficiency (in association with energy
restriction) exerts profound effects on the gut mucosal immune system,
leading to changes in systemically disseminated immune responses and,
importantly, to prolonged parasite survival.
71. Zinc-altered immune function and cytokine production.
Rink L, Kirchner H.
Institute of Immunology and Transfusion Medicine, University of Lubeck
School of Medicine, Lubeck, Germany.
J Nutr. 2000 May;130(5S Suppl):1407S-11S.
Although the intriguing role of zinc as an essential trace element for
immune
function is well established, particular progress in determining the molecular
principles of action of this ion was made recently. Leukocyte responsiveness
is
delicately regulated by zinc concentration. Zinc deficiency as well as
supraphysiologic levels impair immune function. Furthermore, the activities
of
many immunostimulants frequently used in immunologic studies are influenced
by zinc concentration. Therefore, our knowledge from in vitro studies
is widely
dependent on the zinc concentration, and when not in physiologic range,
immunologic responses are artificially low. Decreased production of TH1
cytokines and interferon-alpha by leukocytes in the healthy elderly person
is
correlated with low zinc serum level. The defect in interferon-alpha production
is reconstituted by the addition of physiologic amounts of zinc in vitro.
Interestingly, zinc induces cytokine production by isolated leukocytes.
Zinc
induces monocytes to produce interleukin-1, interleukin-6 and tumor necrosis
factor-alpha in peripheral blood mononuclear cells and separated monocytes.
This effect is higher in serum-free medium. However, only in the presence
of serum does zinc also induce T cells to produce lymphokines. This effect
on T cells is mediated by cytokines produced by monocytes. Stimulation
also requires
cell-to-cell contact of monocytes and T cells. Information is presented
to
illustrate the concepts that the zinc concentration must be taken into
account
whenever in vitro studies are made or complex alterations of immune functions
are observed in vivo.
72. Zinc status and immune system relationship: a review.
Salgueiro MJ, Zubillaga M, Lysionek A, Cremaschi G, Goldman CG, Caro
R, De Paoli T, Hager A, Weill R, Boccio J.
Radioisotope Laboratory, School of Pharmacy and Biochemistry, University
of
Buenos Aires, Argentina.
Biol Trace Elem Res. 2000 Sep;76(3):193-205.
The essentiality of zinc for humans was first documented by Prasad in
the 1960s. The main clinical manifestations associated with zinc deficiency
are growth retardation, hypogonadism, diarrhea, and increased susceptibility
to infectious diseases. Thus, in the past 25 yr, there was an increased
interest of
researchers in studying the role of zinc in human immunity. Although mechanistic
research has been carried out using animal models, there are several studies
in humans with similar results. This work is an attempt to review the
information available in this field to understand the important role that
zinc plays in the normal development and function of the immune system.
73. Effects of zinc deficiency on Th1 and Th2 cytokine shifts.
Prasad AS. Wayne State University, University Health Center, Detroit,
MI 48201, USA. prasada@karmanos.org
J Infect Dis. 2000 Sep;182 Suppl 1:S62-8.
Nutritional deficiency of zinc is widespread throughout developing countries,
and zinc-deficient persons have increased susceptibility to a variety
of pathogens. Zinc deficiency in an experimental human model caused an
imbalance between Th1 and Th2 functions. Production of interferon-gamma
and interleukin (IL)-2 (products of Th1) were decreased, whereas production
of IL-4, IL-6, and IL-10 (products of Th2) were not affected during zinc
deficiency. Zinc deficiency decreased natural killer cell lytic activity
and percentage of precursors of cytolytic T cells. In HuT-78, a Th0 cell
line, zinc deficiency decreased gene expression of thymidine kinase, delayed
cell cycle, and decreased cell growth. Gene expression of IL-2 and IL-2
receptors (both alpha and beta) and binding of NF-kappaB to DNA were decreased
by zinc deficiency in HuT-78. Decreased production of IL-2 in zinc deficiency
may be due to decreased activation of NF-kappaB and subsequent decreased
gene expression of IL-2 and IL-2 receptors.
74. Zinc status in patients with alveolar echinococcosis is related to
disease
progression.
Wellinghausen N, Jochle W, Reuter S, Flegel WA, Grunert A, Kern P.
Section of Infectious Diseases and Clinical Immunology, University of
Ulm,
Robert-Koch-Strasse 8, 89081 Ulm, Germany.
Parasite Immunol. 1999 May;21(5):237-41.
Zinc is an essential trace element for immune function that plays a role
in
immune response against parasites. To determine a possible relationship
between zinc level and disease status in alveolar echinococcosis (AE),
we investigated serum concentrations of zinc, immunoglobulin (Ig)E, IgG,
and C-reactive protein (CRP) in 40 AE patients and 20 controls. Patients
were classified into three groups: group A: patients after curative surgery,
group B: patients with
stabilized disease, group C: patients with progressive disease. Patients
showed
significantly higher levels of IgE and IgG than controls. Amounts of IgE
and IgG
were related to disease severity, achieving highest levels in group C
and lowest
in group A. Zinc levels were comparable in patients and controls. However,
there
was an obvious association between zinc concentration and disease severity.
Zinc was far below the normal range in group C (median 9.2 micromol/l)
and
significantly diminished compared to group B and controls. An inverse
pattern
was seen for CRP. In conclusion, lowered zinc concentration in progressive
cases may be caused by enhanced immune activation but consumption of zinc
by the growing parasite may also play a role. Furthermore, decreased zinc
levels may contribute to the observed immunosuppression in AE.
75. Zinc deficiency: changes in cytokine production and T-cell subpopulations
in patients with head and neck cancer and in noncancer subjects.
Prasad AS; Beck FW; Grabowski SM; Kaplan J; Mathog RH Department of Internal
Medicine, Wayne State University School of Medicine, Detroit, MI
Proc Assoc Am Physicians Jan 1997, 109 (1) p68-77
Cell-mediated immune dysfunctions and susceptibility to infections have
been observed in zinc -deficient human subjects. In this study, we investigated
the production of cytokines and characterized the T-cell subpopulations
in three groups of mildly zinc -deficient subjects. These included head
and neck cancer patients, healthy volunteers who were found to have a
dietary deficiency of zinc, and healthy volunteers in whom we induced
zinc deficiency experimentally by dietary means. We used cellular zinc
criteria for the diagnosis of zinc deficiency. We assayed enzyme-linked
immunosorbent assay the production of cytokines from phytohemagglutinin-stimulated
peripheral blood mononuclear cells and assessed by flow cytometry the
differences in T-cell subpopulations. Our studies showed that the cytokines
produced by TH1 cells were particularly sensitive to zinc status, inasmuch
as the production of interleukin-2 (IL-2) and interferon-gamma were decreased
even though the deficiency of zinc was mild in our subjects. TH2 cytokines
(IL-4, IL-5, and IL-6) were not affected by zinc deficiency. Natural killer
cell lytic activity also was decreased in zinc -deficient subjects. Recruitment
of naive T cells (CD4+CD45 RA+) and CD8+ CD73+ CD11b-, precursors of cytolytic
T cells, were decreased in mildly zinc -deficient subjects. An imbalance
between the functions of TH1 and TH2 cells and changes in T-cell subpopulations
are most probably responsible for cell-mediated immune dysfunctions in
zinc deficiency.
76. Serum thymic factor activity in deficiencies of calories, zinc, vitamin
A and pyridoxine.
Chandra RK, Heresi G, Au B
Clin Exp Immunol 1980 Nov;42(2):332-5
Cell-mediated immunity is invariably impaired in protein-energy malnutrition.
The effect of selected nutrient deficiencies on serum thymic factor activity
was assessed in deprived rats and pair-fed controls. Deficits of calories,
zinc or pyridoxine resulted in significant lowering of serum thymic factor
activity whereas vitamin A deficiency did not have any effect. It is suggested
that variants nutrients modulate different steps of cell-mediated immunity
and that reduced thymic hormone activity may be the underlying mechanism
of impaired immunity in some but not all nutritional deficiencies.
77. Zinc and immune function.
Dardenne M.
CNRS UMR 8603, Universite Paris V, Hopital Necker, Paris, France.
dardenne@necker.fr
Eur J Clin Nutr. 2002 Aug;56 Suppl 3:S20-3.
It is well recognized that zinc is an essential trace element, influencing
growth and affecting the development and integrity of the immune system.
Research has begun to clarify the molecular mechanisms underlying the
action of zinc on the immune function. It is clear that this trace element
has a broad
impact on key immunity mediators, such as enzymes, thymic peptides and
cytokines, explaining the paramount importance of zinc's status on the
regulation of lymphoid cell activation, proliferation and apoptosis. Ongoing
and
future studies regarding the immunological status of zinc deficiency 'at
risk'
groups could lead to public health interventions with nutritional doses
of zinc
supplements to prevent alteration of the immune system and improve resistance
to infections.
78. Preventive nutrition: disease-specific dietary interventions for
older adults.
Johnson K; Kligman EW Dept. of Family and Community Medicine, University
of Arizona College of Medicine, Tucson.
Geriatrics Nov 1992, 47 (11) p39-40, 45-9
Disease prevention through dietary management is a cost-effective approach
to promoting healthy aging. Fats, cholesterol, soluble fiber, and the
trace elements copper and chromium affect the morbidity and mortality
of CHD. Decreasing sodium and increasing potassium intake improves control
of hypertension. Calcium and magnesium may also have a role in controlling
hypertension. The antioxidant vitamins A and beta-carotene, vitamin C,
vitamin E, and the trace mineral selenium may protect against types of
cancer. A decrease in simple carbohydrates and an increase in soluble
dietary fiber may normalize moderately elevated blood glucose levels.
Deficiencies of zinc or iron diminish immune function . Adequate levels
of calcium and vitamin D can help prevent senile osteoporosis in both
older men and women. (27 Refs.)
79. Effects of zinc deficiency on Th1 and Th2 cytokine shifts.
Prasad AS. Wayne State University, University Health Center, Detroit,
MI 48201, USA. prasada@karmanos.org
J Infect Dis. 2000 Sep;182 Suppl 1:S62-8.
Nutritional deficiency of zinc is widespread throughout developing countries,
and zinc-deficient persons have increased susceptibility to a variety
of pathogens. Zinc deficiency in an experimental human model caused an
imbalance between Th1 and Th2 functions. Production of interferon-gamma
and interleukin (IL)-2 (products of Th1) were decreased, whereas production
of IL-4, IL-6, and IL-10 (products of Th2) were not affected during zinc
deficiency. Zinc deficiency decreased natural killer cell lytic activity
and percentage of precursors of cytolytic T cells. In HuT-78, a Th0 cell
line, zinc deficiency decreased gene expression of thymidine kinase, delayed
cell cycle, and decreased cell growth. Gene expression of IL-2 and IL-2
receptors (both alpha and beta) and binding of NF-kappaB to DNA were decreased
by zinc deficiency in HuT-78. Decreased production of IL-2 in zinc deficiency
may be due to decreased activation of NF-kappaB and subsequent decreased
gene expression of IL-2 and IL-2 receptors.
80. Zinc deficiency: changes in cytokine production and T-cell subpopulations
in patients with head and neck cancer and in noncancer subjects.
Prasad AS; Beck FW; Grabowski SM; Kaplan J; Mathog RH Department of Internal
Medicine, Wayne State University School of Medicine, Detroit, MI
Proc Assoc Am Physicians Jan 1997, 109 (1) p68-77
Cell-mediated immune dysfunctions and susceptibility to infections have
been observed in zinc -deficient human subjects. In this study, we investigated
the production of cytokines and characterized the T-cell subpopulations
in three groups of mildly zinc -deficient subjects. These included head
and neck cancer patients, healthy volunteers who were found to have a
dietary deficiency of zinc, and healthy volunteers in whom we induced
zinc deficiency experimentally by dietary means. We used cellular zinc
criteria for the diagnosis of zinc deficiency. We assayed enzyme-linked
immunosorbent assay the production of cytokines from phytohemagglutinin-stimulated
peripheral blood mononuclear cells and assessed by flow cytometry the
differences in T-cell subpopulations. Our studies showed that the cytokines
produced by TH1 cells were particularly sensitive to zinc status, inasmuch
as the production of interleukin-2 (IL-2) and interferon-gamma were decreased
even though the deficiency of zinc was mild in our subjects. TH2 cytokines
(IL-4, IL-5, and IL-6) were not affected by zinc deficiency. Natural killer
cell lytic activity also was decreased in zinc -deficient subjects. Recruitment
of naive T cells (CD4+CD45 RA+) and CD8+ CD73+ CD11b-, precursors of cytolytic
T cells, were decreased in mildly zinc -deficient subjects. An imbalance
between the functions of TH1 and TH2 cells and changes in T-cell subpopulations
are most probably responsible for cell-mediated immune dysfunctions in
zinc deficiency.
81. Zinc deficiency impairs immune responses against parasitic nematode
infections at intestinal and systemic sites.
Scott ME, Koski KG. Institute of Parasitology, School of Dietetics and
Human Nutrition, McGill University, Macdonald Campus, Ste-Anne de Bellevue,
Quebec H9X 3V9, Canada.
J Nutr. 2000 May;130(5S Suppl):1412S-20S.
Research on the complex interactions among host nutritional status, parasitic
infection and immune responsiveness has focused on the detrimental consequences
of parasitic infections on host nutritional status and on mechanisms by
which malnutrition impairs immunocompetence. Curiously, relatively few
studies have examined the effects of malnutrition on the immune response
in the parasite-infected host, and even fewer have considered the events
occurring at the intestinal level, where absorption of nutrients occurs,
intestinal parasites reside, and the gastrointestinal-associated lymphoid
tissues play a role in directing both the local and the more systemic
immune responses. Our work using a zinc-deficient nematode-infected mouse
model reveals that parasites are better able to survive in the zinc-deficient
hosts than in well-nourished hosts; that the production of interleukin-4
in the spleen of zinc-deficient mice is depressed, leading to depressed
levels of IgE, IgG(1) and eosinophils; and that the function of T cells
and antigen-presenting cells is impaired by zinc deficiency as well as
by energy restriction. Given the paramount role of the gastrointestinal-associated
lymphoid tissues in inducing and regulating immune responses to intestinal
parasites and in orchestrating responses in the spleen and peripheral
circulation, we conclude that zinc deficiency (in association with energy
restriction) exerts profound effects on the gut mucosal immune system,
leading to changes in systemically disseminated immune responses and,
importantly, to prolonged parasite survival.
82. Zinc and immune function: the biological basis of altered resistance
to infection.
Shankar AH; Prasad AS Department of International Health, The Johns Hopkins
University School of Public Health, Baltimore, MD 21205, USA. ashankar@jhsph.edu
Am J Clin Nutr Aug 1998, 68 (2 Suppl) p447S-463S
Zinc is known to play a central role in the immune system, and zinc-deficient
persons experience increased susceptibility to a variety of pathogens.
The immunologic mechanisms whereby zinc modulates increased susceptibility
to infection have been studied for several decades. It is clear that zinc
affects multiple aspects of the immune system, from the barrier of the
skin to gene regulation within lymphocytes. Zinc is crucial for normal
development and function of cells mediating nonspecific immunity such
as neutrophils and natural killer cells. Zinc deficiency also affects
development of acquired immunity by preventing both the outgrowth and
certain functions of T lymphocytes such as activation, Th1 cytokine production,
and B lymphocyte help. Likewise, B lymphocyte development and antibody
production, particularly immunoglobulin G, is compromised. The macrophage,
a pivotal cell in many immunologic functions, is adversely affected by
zinc deficiency, which can dysregulate intracellular killing, cytokine
production, and phagocytosis. The effects of zinc on these key immunologic
mediators is rooted in the myriad roles for zinc in basic cellular functions
such as DNA replication, RNA transcription, cell division, and cell activation.
Apoptosis is potentiated by zinc deficiency. Zinc also functions as an
antioxidant and can stabilize membranes. This review explores these aspects
of zinc biology of the immune system and attempts to provide a biological
basis for the altered host resistance to infections observed during zinc
deficiency and supplementation. (271Refs.)
MACULAR
83. Risk factors for age-related macular degeneration: an update.
Hyman L, Neborsky R.
Stony Brook University, Department of Preventive Medicine, Stony Brook,
New York 11794-8036, USA. lhyman@notes.cc.sunysb.edu
Curr Opin Ophthalmol. 2002 Jun;13(3):171-5.
Age-related macular degeneration (AMD) is the leading cause of irreversible
vision loss in the United States and other western nations. Limited treatment
is available, and there are no established means of prevention. The detection
of modifiable risk factors is important to suggest preventive behaviors
that can reduce disease occurrence or prevent the progression to the late
stages of AMD. Results of recent studies suggest that the etiology and
pathogenesis of AMD are a complex interaction of genetic and external
factors. Although a number of factors seem promising, only age and cigarette
smoking are confirmed as
increasing AMD risk. Other factors that most likely play a significant
role in AMD are nutritional factors, e.g., antioxidants, and hypertension
or other underlying atherosclerotic disease processes. The results of
the Age-Related Eye Disease Study suggest a moderate beneficial effect
of antioxidant, vitamin, and zinc supplementation in reducing progression
to severe AMD.
84. [Antioxidants and angiogenetic factor associated with age-related
macular degeneration (exudative type)]
Ishihara N; Yuzawa M; Tamakoshi A
Department of Ophthalmology, Nihon University School of Medicine, Tokyo,
Japan.
Nippon Ganka Gakkai Zasshi (Japan) Mar 1997, 101 (3) p248-51
To confirm the hypothesis that antioxidants and angiogenetic factors
may be associated with the development of age-related macular degeneration
(exudative type), we compared serum levels of vitamins A, C, and E and
carotinoid, zinc, selenium and b-FGF (basic-fibroblast growth factor)
in 35 patients with age-related macular degeneration (exudative type)
with the levels in 66 controls. The average serum zinc level was significantly
lower in the patient group than in the control group. Serum vitamin E-alpha
levels also tended to be lower. Most serum b-FGF levels were below the
standard value in each group. Based on the above results, we conclude
that subnormal levels of zinc and
vitamin E may be associated with the development of age-related macular
degeneration.
85. Nutrition in the elderly.
Morley JE, Mooradian AD, Silver AJ, Heber D, Alfin-Slater RB.
Department of Medicine, University of California School of Medicine, Los
Angeles.
Ann Intern Med. 1988 Dec 1;109(11):890-904.
Nutritional modulation is one approach to successful aging. In animals,
dietary
restriction increases life span. Alterations in the macronutrient and
micronutrient constituent of the diet can modulate gene expression. Anorexia
is
common in elderly persons. The results of studies in animals suggest that
aging
is associated with a decrease in the opioid feeding drive and an increase
in the
satiating effect of cholecystokinin. Unrecognized depression is a common,
treatable cause of anorexia and weight loss in elderly persons. Protein
synthesis decreases in elderly persons; nevertheless, nitrogen balance
can be
maintained in patients with fairly low intakes of protein. Carbohydrate
intolerance is common and may be modulated by nutritional intervention
and
physical activity. The role of cholesterol in the development of heart
disease
in very old persons is controversial. Homebound and institutionalized
elderly
persons often do not expose their skin to sunlight; because the skin of
older
persons has a decreased ability to form vitamin D, the vitamin D status
in these
persons is precarious and they are at risk for osteopenia. Vitamins are
often
abused by elderly persons. Drug administration alters the vitamin requirements
of persons. Borderline zinc state has been associated with deteriorating
immune
function, especially in persons who have diabetes mellitus or who abuse
alcohol.
Zinc administration appears to protect against the deteriorating vision
associated with age-related macular degeneration. Selenium deficiency
seems to
be associated with an increased prevalence of cancer.
OSTEOPOROSIS
86. Increased incidence of fractures in middle-aged and elderly men with
low intakes of phosphorus and zinc.
Elmstahl S, Gullberg B, Janzon L, Johnell O, Elmstahl B.
Department of Community Medicine, Lund University, Malmo, Sweden.
solve.elmstahl@smi.mas.lu.se
Osteoporos Int. 1998;8(4):333-40.
The aim of the study was to determine dietary risk factors for fracture
in men
aged 46-68 years. Six thousand five hundred and seventy-six men were randomly
invited using the Municipal Registry to a diet and health study. The diet
was assessed using a combined 7-day menu book for hot meals, beverages
and dietary supplements and a quantitative food frequency questionnaire
for other foods. The fracture incidence was 103/10,000 person-years during
a mean follow-up of 2.4 years. Zinc and phosphorus intake were associated
with fracture risk and showed a threshold effect. The zinc intake in the
lowest decentile, 10 mg daily, was associated with almost a doubled risk
of fracture compared with the fourth and fifth quintiles (RR = 0.47; 95%
confidence interval, 27-82) of zinc intake adjusted for energy, previous
fractures, lifestyle factors and co-morbidity.
Energy-adjusted phosphorus intake in the lowest quintile, mean level 1357
mg,
was associated with an increased fracture risk compared with subjects
in the
second quintile. Smoking, martial status and physical activity were
independently associated with fracture risk. Calcium, retinol and vitamin
D
showed no associations with fracture risk. We conclude that inadequate
intakes
of zinc and phosphorus are important risk factors for fracture.
PARKINSON’S DISEASE
87. Evidence of functional zinc deficiency in Parkinson's disease.
Forsleff L, Schauss AG, Bier ID, Stuart S.
School of Community Health Service, Western Michigan University, Kalamazoo,
USA.
J Altern Complement Med. 1999 Feb;5(1):57-64.
One of the primary areas of investigation in the pathophysiology of Parkinson's
disease (PD) is the loss of the dopamine-producing cells in the melanized
neurons of the substantia nigra, believed to be caused by oxidative stress
resulting from excessive free radical activity. The cuprozinc enzyme,
superoxide
dismutase (SODCu2Zn2), catalyzes the dismutation of superoxide anions
to
hydrogen peroxide plus oxygen, and is normally found in high concentrations
in
the substantia nigra where it protects neurons by scavenging free radicals.
Zinc
supplementation has been shown to significantly increase SODCu2Zn2 in
vitro. A
novel oral zinc tally test (ZTT) used in the assessment of zinc status
was
administered to 100 PD patients and 25 controls. Patients with PD showed
a
significantly decreased zinc status as compared to controls (p < 0.001).
Significance was also established for 3 self-reported health-related variables
thought to be related to zinc status: vision problems, olfactory loss,
and taste
loss (p < 0.05). Relative risks for patients with PD for these variables
were
1.51, 1.56, and 1.33, respectively. Zinc status as measured by the ZTT
is
negatively correlated with PD status. PD status is positively correlated
with
self-reported vision problems, and olfactory and taste loss. Further study
of
the role of zinc in the development and treatment of PD is warranted.
PROSTATE
88. Carcinogenicity of oral cadmium in the male Wistar (WF/NCr) rat:
Effect of chronic dietary zinc deficiency
Waalkes M.P.; Rehm S.
Lab. of Comparative Carcinogenesis, NCI-FCRDC, Frederick, MD 21702-1201
USA
Fundam. Aappl Toxicol. (USA), 1992, 19/4 (512-520)
The effect of chronic dietary zinc deficiency on the carcinogenic potential
of dietary cadmium was assessed in male Wistar (WF/NCr) rats. Groups (n
= 28) of rats were fed diets adequate (60 ppm) or marginally deficient
(7 ppm) in zinc and containing cadmium at various levels (0, 25, 50, 100,
or 200 ppm). Lesions were assessed over the following 77 weeks. Zinc deficiency
alone had no effect on survival, growth, or food consumption. Cadmium
treatment did not reduce survival or food consumption and only at the
highest doses of cadmium (100 and 200 ppm) was body weight reduced (maximum
17%). The incidence of prostatic proliferative lesions, both hyperplasias
and adenomas, was increased over that seen in controls (1.8%) in both
zinc-adequate (20%) and zinc-deficient rats (14%) fed 50 ppm cadmium.
The overall incidence for prostatic lesions for all cadmium treatment
groups was, however, much lower in zinc-deficient rats, possibly because
of a marked increase in prostatic atrophy that was associated with reduced
zinc intake. Cadmium treatment resulted in an elevated leukemia incidence
(maximum 4.8-fold over control) in both zinc-adequate and zinc-deficient
groups, although zinc deficiency reduced the potency of cadmium in this
respect. Testicular tumors were significantly elevated only in rats receiving
200 ppm cadmium and diets adequate in zinc. Both zinc-deficient and zinc-adequate
groups showed significant positive trends for development of testicular
neoplasia with increasing cadmium dosage. Thus, oral cadmium exposure
is clearly associated with tumors of the prostate, testes, and hematopoietic
system in rats, while dietary zinc deficiency has complex, apparently
inhibitory, effects on cadmium carcinogenesis by this route.
89. Zinc, vitamin A and prostatic cancer
Whelan P.; Walker B.E.; Kelleher J.
Dep. Urol., St. James's Univ. Hosp., Leeds LS9 7TF United Kingdom
Br. J. Urol. (England), 1983, 55/5 (525-528)
The serum zinc, vitamin A, albumin, copper and retinoid-binding protein
content was measured in 27 patients with benign prostatic hyperplasia
and 19 patients with carcinoma of the prostate. A significantly lower
(P = < 0.05) level of serum zinc was found in the cancer group as well
as a significant zinc/vitamin A correlation (P = < 0.05). The possible
significance of this in relation to the pathogenesis of carcinoma of the
prostate is discussed.
SKIN AGING
90. Evidence supporting zinc as an important antioxidant for skin.
Rostan EF, DeBuys HV, Madey DL, Pinnell SR.
Duke University, Durham, NC 27710, USA.
Int J Dermatol. 2002 Sep;41(9):606-11.
Antioxidants play a critical role in keeping skin healthy. The antioxidant
benefits of vitamin C and E are well known, but the importance of the
trace
mineral, zinc, has been overlooked. This article reviews the evidence
supporting
zinc's antioxidant role in protecting against free radical-induced oxidative
damage. Zinc protects against UV radiation, enhances wound healing, contributes
to immune and neuropsychiatric functions, and decreases the relative risk
of cancer and cardiovascular disease. All body tissues contain zinc; in
skin, it is five to six times more concentrated in the epidermis than
the dermis. Zinc is
required for the normal growth, development and function of mammals. It
is an
essential element of more than 200 metalloenzymes, including the antioxidant
enzyme, superoxide dismutase, and affects their conformity, stability,
and
activity. Zinc also is important for the proper functioning of the immune
system, and for glandular, reproductive and cell health. Abundant evidence
demonstrates the antioxidant role of zinc. Topical zinc, in the form of
divalent
zinc ions, has been reported to provide antioxidant photoprotection for
skin.
Two antioxidant mechanisms have been proposed for zinc: zinc ions may
replace
redox active molecules, such as iron and copper, at critical sites in
cell
membranes and proteins; alternatively, zinc ions may induce the synthesis
of
metallothionein, sulfhydryl-rich proteins that protect against free radicals.
No
matter how they work, topical zinc ions may provide an important and helpful
antioxidant defense for skin.
Wound Healing
91. The role of zinc in wound healing.
Andrews M, Gallagher-Allred C. Geriatric and Long Term Care Services,
Ross Products Division, Abbott Laboratories, Columbus, OH, USA.
Adv Wound Care 1999 Apr;12(3):137-8
Zinc deficiency has been associated with delayed wound healing. Because
zinc deficiency may be common in the United States, foods rich in zinc,
as well as all other essential nutrients, should be promoted in the diet
of patients who are malnourished or at risk for malnutrition.
Effects of exogenous zinc supplementation on intestinal epithelial repair
in vitro.
Cario E, Jung S, Harder D'Heureuse J, Schulte C, Sturm A, Wiedenmann B,
Goebell H, Dignass AU. University of Essen, Essen, Germany; Charite Medical
School-Campus Virchow, Berlin, Germany.
Eur J Clin Invest 2000 May;30(5):419-28
BACKGROUND: Substitution of zinc modulates antioxidant capabilities within
the intestinal mucosa and improves intestinal wound healing in zinc-deficient
patients with inflammatory bowel diseases. The aim of this study was to
characterize the modulating effects of zinc on intestinal epithelial cell
function in vitro. MATERIALS AND METHODS: The effects of zinc on intestinal
epithelial cell morphology were assessed by phase contrast and transmission
electron microscopy using the non-transformed small intestinal epithelial
cell line IEC-6. Zinc-induced apoptosis was assessed by DNA fragmentation
analysis, lactate dehydrogluase (LDH) release and flow cytometry with
propidium iodine staining. Furthermore, the effects of zinc on IEC-6 cell
proliferation were assessed using a colorimetric thiazolyl blue (MTT)
assay and on IEC-6 cell restitution using an in vitro wounding model.
RESULTS: Physiological concentrations of zinc (25 microM) did not significantly
alter the morphological appearance of IEC-6 cells. However, a 10-fold
higher dose of zinc (250 microM) induced epithelial cell rounding, loss
of adherence and apoptotic characteristics. While physiological zinc concentrations
(< 100 microM) did not induce apoptosis, supraphysiological zinc concentrations
(> 100 microM) caused apoptosis. Physiological concentrations of zinc
(6.25-50 microM) had no significant effect on intestinal epithelial cell
proliferation. In contrast, physiological concentrations of zinc (12.5-50
microM) significantly enhanced epithelial cell restitution through a transforming
growth factor-beta (TGFbeta)-independent mechanism. Simultaneous addition
of TGFbeta and zinc resulted in an additive stimulation of IEC-6 cell
restitution. CONCLUSION: Zinc may promote intestinal epithelial wound
healing by enhancement of epithelial cell restitution, the initial step
of epithelial wound healing. Zinc supplementation may improve epithelial
repair; however, excessive amounts
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1: Nowak G, Szewczyk B, Wieronska JM, Branski P, Palucha A, Pilc A, Sadlik K, Piekoszewski W. Antidepressant-like effects of acute and chronic treatment with zinc in forced swim test and olfactory bulbectomy model in rats. Brain Res Bull. 2003 Jul 15;61(2):159-64. PMID: 12832002
2: Lambert JC, Zhou Z, Wang L, Song Z, McClain CJ, Kang YJ. Prevention of alterations in intestinal permeability is involved in zinc inhibition of acute ethanol-induced liver damage in mice. J Pharmacol Exp Ther. 2003 Jun;305(3):880-6. Epub 2003 Mar 06. PMID: 12626662
3: Roldan S, Winkel EG, Herrera D, Sanz M, Van Winkelhoff AJ. The effects of a new mouthrinse containing chlorhexidine, cetylpyridinium chloride and zinc lactate on the microflora of oral halitosis patients: a dual-centre, double-blind placebo-controlled study. J Clin Periodontol. 2003 May;30(5):427-34. PMID: 12716335
4: Winkel EG, Roldan S, Van Winkelhoff AJ, Herrera D, Sanz M. Clinical effects of a new mouthrinse containing chlorhexidine, cetylpyridinium chloride and zinc-lactate on oral halitosis. A dual-center, double-blind placebo-controlled study. J Clin Periodontol. 2003 Apr;30(4):300-6. PMID: 12694427
5: Orbak R, Cicek Y, Tezel A, Dogru Y. Effects of zinc treatment in patients with recurrent aphthous stomatitis. Dent Mater J. 2003 Mar;22(1):21-9. PMID: 12790293
6: Mossad SB. Effect of zincum gluconicum nasal gel on the duration and symptom severity of the common cold in otherwise healthy adults. QJM. 2003 Jan;96(1):35-43. PMID: 12509647
7: McElroy BH, Miller SP. Effectiveness of zinc gluconate glycine lozenges (Cold-Eeze) against the common cold in school-aged subjects: a retrospective chart review. Am J Ther. 2002 Nov-Dec;9(6):472-5. PMID: 12424502
8: Nowak G, Szewczyk B. Mechanisms contributing to antidepressant zinc actions. Pol J Pharmacol. 2002 Nov-Dec;54(6):587-92. Review. PMID: 12866713
9: Putt MS, Yu D, Kohut BE. Inhibition of calculus formation by dentifrice formulations containing essential oils and zinc. Am J Dent. 2002 Oct;15(5):335-8. PMID: 12537346
10: Rostan EF, DeBuys HV, Madey DL, Pinnell SR. Evidence supporting zinc as an important antioxidant for skin. Int J Dermatol. 2002 Sep;41(9):606-11. Review. PMID: 12358835
11: Bhandari N, Bahl R, Taneja S, Strand T, Molbak K, Ulvik RJ, Sommerfelt H, Bhan MK. Effect of routine zinc supplementation on pneumonia in children aged 6 months to 3 years: randomised controlled trial in an urban slum. BMJ. 2002 Jun 8;324(7350):1358. PMID: 12052800
12: Oken E, Duggan C. Update on micronutrients: iron and zinc. Curr Opin Pediatr. 2002 Jun;14(3):350-3. Review. PMID: 12011679
13: Cho YH, Lee SJ, Lee JY, Kim SW, Lee CB, Lee WY, Yoon MS. Antibacterial effect of intraprostatic zinc injection in a rat model of chronic bacterial prostatitis. Int J Antimicrob Agents. 2002 Jun;19(6):576-82. PMID: 12135851
14: Bhandari N, Bahl R, Taneja S, Strand T, Molbak K, Ulvik RJ, Sommerfelt H, Bhan MK. Substantial reduction in severe diarrheal morbidity by daily zinc supplementation in young north Indian children. Pediatrics. 2002 Jun;109(6):e86. PMID: 12042580
15: Strand TA, Chandyo RK, Bahl R, Sharma PR, Adhikari RK, Bhandari N, Ulvik RJ, Molbak K, Bhan MK, Sommerfelt H. Effectiveness and efficacy of zinc for the treatment of acute diarrhea in young children. Pediatrics. 2002 May;109(5):898-903. PMID: 11986453
16: Lowe NM, Lowe NM, Fraser WD, Jackson MJ. Is there a potential therapeutic value of copper and zinc for osteoporosis? Proc Nutr Soc. 2002 May;61(2):181-5. Review. PMID: 12133199
17: Karyadi E, West CE, Schultink W, Nelwan RH, Gross R, Amin Z, Dolmans WM, Schlebusch H, van der Meer JW. A double-blind, placebo-controlled study of vitamin A and zinc supplementation in persons with tuberculosis in Indonesia: effects on clinical response and nutritional status. Am J Clin Nutr. 2002 Apr;75(4):720-7. PMID: 11916759
18: Afonne OJ, Orisakwe OE, Obi E, Dioka CE, Ndubuka GI. Nephrotoxic actions of low-dose mercury in mice: protection by zinc. Arch Environ Health. 2002 Mar-Apr;57(2):98-102. PMID: 12194165
19: Hwang IK, Go VL, Harris DM, Yip I, Song MK. Effects of arachidonic acid plus zinc on glucose disposal in genetically diabetic (ob/ob) mice. Diabetes Obes Metab. 2002 Mar;4(2):124-31. PMID: 11940110
20: Su JC, Birmingham CL. Zinc supplementation in the treatment of anorexia nervosa. Eat Weight Disord. 2002 Mar;7(1):20-2. Review. PMID: 11930982
21: Tsocheva-Gaitandjieva NT, Gabrashanska MP, Tepavitcharova S. Trace element levels in the liver of rats with acute and chronic fascioliasis and after treatment with zinc-copper hydroxochloride mixed crystals. J Helminthol. 2002 Mar;76(1):87-90. PMID: 12018202
22: Zemel BS, Kawchak DA, Fung EB, Ohene-Frempong K, Stallings VA. Effect of zinc supplementation on growth and body composition in children with sickle cell disease. Am J Clin Nutr. 2002 Feb;75(2):300-7. PMID: 11815322
23: Yoshida S, Tomita H. A case of Cronkhite-Canada syndrome whose major complaint, taste disturbance, was improved by zinc therapy. Acta Otolaryngol Suppl. 2002;(546):154-8. PMID: 12132614
24: Rahman MM, Wahed MA, Fuchs GJ, Baqui AH, Alvarez JO. Synergistic effect of zinc and vitamin A on the biochemical indexes of vitamin A nutrition in children. Am J Clin Nutr. 2002 Jan;75(1):92-8. PMID: 11756065
25: Prasad AS, Kucuk O. Zinc in cancer prevention. Cancer Metastasis Rev. 2002;21(3-4):291-5. Review. PMID: 12549767
26: Yoshida Y, Higashi T, Nouso K, Nakatsukasa H, Nakamura SI, Watanabe A, Tsuji T. Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with decompensated liver cirrhosis. Acta Med Okayama. 2001 Dec;55(6):349-55. PMID: 11779097
27: Jampol LM, Ferris FL 3rd. Antioxidants and zinc to prevent progression of age-related macular degeneration. JAMA. 2001 Nov 21;286(19):2466-8. No abstract available. PMID: 11759670
28: Dijkhuizen MA, Wieringa FT, West CE, Martuti S, Muhilal. Effects of iron and zinc supplementation in Indonesian infants on micronutrient status and growth. J Nutr. 2001 Nov;131(11):2860-5. PMID: 11694609
29: Fong LY, Nguyen VT, Farber JL. Esophageal cancer prevention in zinc-deficient rats: rapid induction of apoptosis by replenishing zinc. J Natl Cancer Inst. 2001 Oct 17;93(20):1525-33. PMID: 11604475
30: Takagi H, Nagamine T, Abe T, Takayama H, Sato K, Otsuka T, Kakizaki S, Hashimoto Y, Matsumoto T, Kojima A, Takezawa J, Suzuki K, Sato S, Mori M. Zinc supplementation enhances the response to interferon therapy in patients with chronic hepatitis C. J Viral Hepat. 2001 Sep;8(5):367-71. PMID: 11555194
31: Christian P, Khatry SK, Yamini S, Stallings R, LeClerq SC, Shrestha SR, Pradhan EK, West KP Jr. Zinc supplementation might potentiate the effect of vitamin A in restoring night vision in pregnant Nepalese women. Am J Clin Nutr. 2001 Jun;73(6):1045-51. PMID: 11382658
32: Najda J, Stella-Holowiecka B, Machalski M. Low-dose zinc administration as an effective Wilson's disease treatment. Biol Trace Elem Res. 2001 Jun;80(3):281-4. PMID: 11508632
33: Iitaka M, Kakinuma S, Fujimaki S, Oosuga I, Fujita T, Yamanaka K, Wada S, Katayama S. Induction of apoptosis and necrosis by zinc in human thyroid cancer cell lines. J Endocrinol. 2001 May;169(2):417-24. PMID: 11312158
34: Yang HM, Chai JK, Guo ZR. [Effect of improved topical agents on healing time of deep second-degree burn wound] Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2001 May;15(3):162-4. Chinese. PMID: 11393958
35: Khatun UH, Malek MA, Black RE, Sarkar NR, Wahed MA, Fuchs G, Roy SK. A randomized controlled clinical trial of zinc, vitamin A or both in undernourished children with persistent diarrhea in Bangladesh. Acta Paediatr. 2001 Apr;90(4):376-80. PMID: 11332926
36: Yoshikawa Y, Ueda E, Miyake H, Sakurai H, Kojima Y. Insulinomimetic bis(maltolato)zinc(II) complex: blood glucose normalizing effect in KK-A(y) mice with type 2 diabetes mellitus. Biochem Biophys Res Commun. 2001 Mar16;281(5):1190-3. PMID: 11243860
37: Hotz C, Brown KH. Identifying populations at risk of zinc deficiency: the use of supplementation trials. Nutr Rev. 2001 Mar;59(3 Pt 1):80-4. Review. PMID: 11330625
38: Ho E, Quan N, Tsai YH, Lai W, Bray TM. Dietary zinc supplementation inhibits NFkappaB activation and protects against chemically induced diabetes in CD1 mice. Exp Biol Med (Maywood). 2001 Feb;226(2):103-11. PMID: 11446433
39: Dreno B, Moyse D, Alirezai M, Amblard P, Auffret N, Beylot C, Bodokh I, Chivot M, Daniel F, Humbert P, Meynadier J, Poli F; Acne Research and Study Group. Multicenter randomized comparative double-blind controlled clinical trial of the safety and efficacy of zinc gluconate versus minocycline hydrochloride in the treatment of inflammatory acne vulgaris. Dermatology. 2001;203(2):135-40. PMID: 11586012
40: Bhutta ZA, Bird SM, Black RE, Brown KH, Gardner JM, Hidayat A, Khatun F, Martorell R, Ninh NX, Penny ME, Rosado JL, Roy SK, Ruel M, Sazawal S, Shankar A. Therapeutic effects of oral zinc in acute and persistent diarrhea in children in developing countries: pooled analysis of randomized controlled trials. Am J Clin Nutr. 2000 Dec;72(6):1516-22. PMID: 11101480
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245: Thyresson N. Acrodermatitis enteropathica. Report of a case healed with zinc therapy. Acta Derm Venereol. 1974;54(5):383-5. No abstract available. PMID: 4138201
246: Fong LY, Mancini R, Nakagawa H, Rustgi AK, Huebner K. Combined cyclin D1 overexpression and zinc deficiency disrupts cell cycle and accelerates mouse forestomach carcinogenesis. Cancer Res. 2003 Jul 15;63(14):4244-52. PMID: 12874033
247: Roth HP. Development of alimentary zinc deficiency in growing rats is retarded at low dietary protein levels. J Nutr. 2003 Jul;133(7):2294-301. PMID: 12840196
248: Levenson CW. Zinc regulation of food intake: new insights on the role of neuropeptide Y. Nutr Rev. 2003 Jul;61(7):247-9. Review. PMID: 12918877
249: Cui H, Jing F, Xi P. Pathology of the thymus, spleen and bursa of Fabricius in zinc-deficient ducklings. Avian Pathol. 2003 Jun;32(3):259-64. PMID: 12850914
250: Takeda A, Hirate M, Tamano H, Nisibaba D, Oku N. Susceptibility to kainate-induced seizures under dietary zinc deficiency. J Neurochem. 2003 Jun;85(6):1575-80. PMID: 12787076
251: Siklar Z, Tuna C, Dallar Y, Tanyer G. Zinc deficiency: a contributing factor of short stature in growth hormone deficient children. J Trop Pediatr. 2003 Jun;49(3):187-8. PMID: 12848213
252: Takeda A, Hirate M, Tamano H, Oku N. Release of glutamate and GABA in the hippocampus under zinc deficiency. J Neurosci Res. 2003 May 15;72(4):537-42. PMID: 12704815
253: Black MM. The evidence linking zinc deficiency with children's cognitive and motor functioning. J Nutr. 2003 May;133(5 Suppl 1):1473S-6S. Review. PMID: 12730446
254: Black RE. Zinc deficiency, infectious disease and mortality in the developing world. J Nutr. 2003 May;133(5 Suppl 1):1485S-9S. Review. PMID: 12730449
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256: Strand TA, Hollingshead SK, Julshamn K, Briles DE, Blomberg B, Sommerfelt H. Effects of zinc deficiency and pneumococcal surface protein a immunization on zinc status and the risk of severe infection in mice. Infect Immun. 2003 Apr;71(4):2009-13. PMID: 12654820
257: tom Dieck H, Doring F, Roth HP, Daniel H. Changes in rat hepatic gene expression in response to zinc deficiency as assessed by DNA arrays. J Nutr. 2003 Apr;133(4):1004-10. PMID: 12672911
258: Sriniwas, Awasthi S, Kumar S, Srivastav RC. Plasma zinc levels in early infancy in north India. Indian Pediatr. 2003 Mar;40(3):235-8. PMID: 12657757
259: Ochi K, Kinoshita H, Kenmochi M, Nishino H, Ohashi T. Zinc deficiency and tinnitus. Auris Nasus Larynx. 2003 Feb;30 Suppl:S25-8. PMID: 12543156
260: Biringen Loker G, Ugur M, Yildiz M. A partial supplementation of pasteurized milk with vitamin C, iron and zinc. Nahrung. 2003 Feb;47(1):17-20. PMID: 12653430
261: Chu Y, Mouat MF, Coffield JA, Orlando R, Grider A. Expression of P2X6, a purinergic receptor subunit, is affected by dietary zinc deficiency in rat hippocampus. Biol Trace Elem Res. 2003 Jan;91(1):77-87. PMID: 12713031
262: Abiaka C, Olusi S, Al-Awadhi A. Reference ranges of copper and zinc and the prevalence of their deficiencies in an Arab population aged 15-80 years. Biol Trace Elem Res. 2003 Jan;91(1):33-43. PMID: 12713027
263: Fong LY, Ishii H, Nguyen VT, Vecchione A, Farber JL, Croce CM, Huebner K. p53 deficiency accelerates induction and progression of esophageal and forestomach tumors in zinc-deficient mice. Cancer Res. 2003 Jan 1;63(1):186-95. PMID: 12517797
264: Baum MK, Campa A, Lai S, Lai H, Page JB. Zinc status in human immunodeficiency virus type 1 infection and illicit drug use. Clin Infect Dis. 2003;37 Suppl 2:S117-23. PMID: 12942385
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268: Ho E, Ames BN. Low intracellular zinc induces oxidative DNA damage, disrupts p53, NFkappa B, and AP1 DNA binding, and affects DNA repair in a rat glioma cell line. Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16770-5. Epub 2002 Dec 12. PMID: 12481036
269: Li Y, Yu ZL. Effect of zinc on bone metabolism in fetal mouse limb culture. Biomed Environ Sci. 2002 Dec;15(4):323-9. PMID: 12642989
270: Kurihara N, Yanagisawa H, Sato M, Tien CK, Wada O. Increased renal vascular resistance in zinc-deficient rats: role of nitric oxide and superoxide. Clin Exp Pharmacol Physiol. 2002 Dec;29(12):1096-104. PMID: 12390298
271: Kanazawa S, Kitaoka T, Ueda Y, Gong H, Amemiya T. Interaction of zinc and vitamin A on the ocular surface. Graefes Arch Clin Exp Ophthalmol. 2002 Dec;240(12):1011-21. Epub 2002 Nov 19. PMID: 12483324
272: Yeiser EC, Vanlandingham JW, Levenson CW. Moderate zinc deficiency increases cell death after brain injury in the rat. Nutr Neurosci. 2002 Oct;5(5):345-52. PMID: 12385597
273: Perafan-Riveros C, Franca LF, Alves AC, Sanches JA Jr. Acrodermatitis enteropathica: case report and review of the literature. Pediatr Dermatol. 2002 Sep-Oct;19(5):426-31. Review. PMID: 12383101
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281: Gomez NN, Ojeda MS, Gimenez MS. Lung lipid composition in zinc-deficient rats. Lipids. 2002 Mar;37(3):291-6. PMID: 11942480
282: Vora RM, Tullu MS, Bartakke SP, Kamat JR. Infantile tremor syndrome and zinc deficiency. Indian J Med Sci. 2002 Feb;56(2):69-72. PMID: 12508616
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286: Tanaka M. Secretory function of the salivary gland in patients with taste disorders or xerostomia: correlation with zinc deficiency. Acta Otolaryngol Suppl. 2002;(546):134-41. PMID: 12132611
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288: Gibson RS, Heath AL, Ferguson EL. Risk of suboptimal iron and zinc nutriture among adolescent girls in Australia and New Zealand: causes, consequences, and solutions. Asia Pac J Clin Nutr. 2002;11 Suppl 3:S543-52. Review. PMID: 12492646
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292: Kechrid Z, Bouzerna N, Zio MS. Effect of low zinc diet on (65)Zn turnover in non-insulin dependent diabetic mice. Diabetes Metab. 2001 Nov;27(5 Pt 1):580-3. PMID: 11694857
293: El Hendy HA, Yousef MI, Abo El-Naga NI. Effect of dietary zinc deficiency on hematological and biochemical parameters and concentrations of zinc, copper, and iron in growing rats. Toxicology. 2001 Oct 15;167(2):163-70. PMID: 11567779
294: Ott ES, Shay NF. Zinc deficiency reduces leptin gene expression and leptin secretion in rat adipocytes. Exp Biol Med (Maywood). 2001 Oct;226(9):841-6. PMID: 11568307
295: Zhao C, Yang H, Jiang H, Han X. [Effects of zinc deficiency on the distribution of elements in the tissue of pregnant rats and their fetuses] Wei Sheng Yan Jiu. 2001 Sep;30(5):277-9. Chinese. PMID: 12561592
296: Nodera M, Yanagisawa H, Wada O. Increased apoptosis in a variety of tissues of zinc-deficient rats. Life Sci. 2001 Aug 24;69(14):1639-49. PMID: 11589504
297: Mahmoodi MR, Kimiagar SM. Prevalence of zinc deficiency in junior high school students of Tehran City. Biol Trace Elem Res. 2001 Aug;81(2):93-103. PMID: 11554399
298: Strand TA, Briles DE, Gjessing HK, Maage A, Bhan MK, Sommerfelt H. Pneumococcal pulmonary infection, septicaemia and survival in young zinc-depleted mice. Br J Nutr. 2001 Aug;86(2):301-6. PMID: 11502245
299: Wang FD, Bian W, Kong LW, Zhao FJ, Guo JS, Jing NH. Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice. Cell Res. 2001 Jun;11(2):135-41. PMID: 11453545
300: Srinivas M, Gupta DK, Rathi SS, Grover JK, Vats V, Sharma JD, Mitra DK. Association between lower hair zinc levels and neural tube defects. Indian J Pediatr. 2001 Jun;68(6):519-22. PMID: 11450382
301: Seshadri S. Prevalence of micronutrient deficiency particularly of iron, zinc and folic acid in pregnant women in South East Asia. Br J Nutr. 2001 May;85 Suppl 2:S87-92. Review. PMID: 11509095
302: Black RE, Sazawal S. Zinc and childhood infectious disease morbidity and mortality. Br J Nutr. 2001 May;85 Suppl 2:S125-9. Review. PMID: 11509100
303: Bhatnagar S, Taneja S. Zinc and cognitive development. Br J Nutr. 2001 May;85 Suppl 2:S139-45. Review. PMID: 11509102
304: Wellinghausen N. Immunobiology of gestational zinc deficiency. Br J Nutr. 2001 May;85 Suppl 2:S81-6. Review. PMID: 11509094
305: Chou HC, Chien CL, Huang HL, Lu KS. Effects of zinc deficiency on the vallate papillae and taste buds in rats. J Formos Med Assoc. 2001 May;100(5):326-35. PMID: 11432312
306: Gong H, Amemiya T. Optic nerve changes in zinc-deficient rats. Exp Eye Res. 2001 Apr;72(4):363-9. PMID: 11273664
307: Grahn BH, Paterson PG, Gottschall-Pass KT, Zhang Z. Zinc and the eye. J Am Coll Nutr. 2001 Apr;20(2 Suppl):106-18. Review. PMID: 11349933
308: Penkowa M, Giralt M, Thomsen PS, Carrasco J, Hidalgo J. Zinc or copper deficiency-induced impaired inflammatory response to brain trauma may be caused by the concomitant metallothionein changes. J Neurotrauma. 2001 Apr;18(4):447-63. PMID: 11336445
309: Rossi L, Migliaccio S, Corsi A, Marzia M, Bianco P, Teti A, Gambelli L, Cianfarani S, Paoletti F, Branca F. Reduced growth and skeletal changes in zinc-deficient growing rats are due to impaired growth plate activity and inanition. J Nutr. 2001 Apr;131(4):1142-6. PMID: 11285316
310: Satre MA, Jessen KA, Clegg MS, Keen CL. Retinol binding protein expression is induced in HepG2 cells by zinc deficiency. FEBS Lett. 2001 Mar 2;491(3):266-71. PMID: 11240140
311: Goto T, Komai M, Suzuki H, Furukawa Y. Long-term zinc deficiency decreases taste sensitivity in rats. J Nutr. 2001 Feb;131(2):305-10. PMID: 11160551
312: Keller KA, Grider A, Coffield JA. Age-dependent influence of dietary zinc restriction on short-term memory in male rats. Physiol Behav. 2001 Feb;72(3):339-48. PMID: 11274675
313: Mori T, Tani T, Hanasawa K, Kodama M. Effects of zinc deficiency and corticosterone elevation on bone marrow in rats. Eur Surg Res. 2001;33(2):92-8. PMID: 11399875
314: Chernekhovskaia NE, Galaeva EV. [Zinc's biological in the pathogenesis of duodenal ulcer] Ross Gastroenterol Zh. 2001;(1):30-4. Review. Russian. PMID: 11565120
315: Micheletti A, Rossi R, Rufini S. Zinc status in athletes: relation to diet and exercise. Sports Med. 2001;31(8):577-82. Review. PMID: 11475319
316: Lorentzen HF, Fugleholm AM, Weismann K. [Zinc deficiency and pellagra in alcohol abuse] Ugeskr Laeger. 2000 Dec 11;162(50):6854-6. Danish. PMID: 11187143
317: Altuntas B, Filik B, Ensari A, Zorlu P, Tezic T. Can zinc deficiency be used as a marker for the diagnosis of celiac disease in Turkish children with short stature? Pediatr Int. 2000 Dec;42(6):682-4. PMID: 11192528
318: Leon-Espinosa de los Monteros MT, Gil Extremera B, Maldonado Martin A, Luna del Castillo JD, Munoz Parra F, Ruiz Lopez MF, Huertas Hernandez F, Cobo Martinez F. [Zinc and chronic obstructive pulmonary disease] Rev Clin Esp. 2000 Dec;200(12):649-53. Spanish. PMID: 11234469
319: Samman S. Is zinc an important nutrient for women aged 40 and over? Med J Aust. 2000 Nov 6;173 Suppl:S98-9. PMID: 11149377
320: Agrawal R, Bedwal RS. SDS-PAGE analysis of caput epididymis proteins in rats receiving a zinc deficient diet. Indian J Exp Biol. 2000 Nov;38(11):1104-10. PMID: 11395953
321: Sahin G, Ertem U, Duru F, Birgen D, Yuksek N. High prevelance of chronic magnesium deficiency in T cell lymphoblastic leukemia and chronic zinc deficiency in children with acute lymphoblastic leukemia and malignant lymphoma. Leuk Lymphoma. 2000 Nov;39(5-6):555-62. PMID: 11342338
322: Rink L, Gabriel P. Zinc and the immune system. Proc Nutr Soc. 2000 Nov;59(4):541-52. Review. PMID: 11115789
323: Mazzocchi C, Michel JL, Chalencon V, Teyssier G, Rayet I, Cambazard F. [Zinc deficiency in mucoviscidosis] Arch Pediatr. 2000 Oct;7(10):1081-4. French. PMID: 11075264
324: Taylor CG, Giesbrecht JA. Dietary zinc deficiency and expression of T lymphocyte signal transduction proteins. Can J Physiol Pharmacol. 2000 Oct;78(10):823-8. Review. PMID: 11077983
325: Yanagisawa H, Moridaira K, Wada O. Zinc deficiency further increases the enhanced expression of endothelin-1 in glomeruli of the obstructed kidney. Kidney Int. 2000 Aug;58(2):575-86. PMID: 10916081
326: Li F, Guo Z, Zhao L. [The effects of zinc supplementation on postburn nutritional status of zinc-deficient scalded rats] Zhonghua Shao Shang Za Zhi. 2000 Aug;16(4):203-5. Chinese. PMID: 11876870
327: Singer LJ, Herron A, Altman N. Zinc responsive dermatopathy in goats: two field cases. Contemp Top Lab Anim Sci. 2000 Jul;39(4):32-5. PMID: 11487227
328: Gupta RP, Verma PC, Garg SR. Effect of experimental zinc deficiency on immunological responses in Salmonella-infected guinea-pigs. J Comp Pathol. 2000 Jul;123(1):1-6. PMID: 10906249
329: Hyun HJ, Sohn J, Ahn YH, Shin HC, Koh JY, Yoon YH. Depletion of intracellular zinc induces macromolecule synthesis- and caspase-dependent apoptosis of cultured retinal cells. Brain Res. 2000 Jun 30;869(1-2):39-48. PMID: 10865057
330: Gibson RS. Zinc supplementation for infants. Lancet. 2000 Jun 10;355(9220):2008-9. PMID: 10885346
331: Keller KA, Chu Y, Grider A, Coffield JA. Supplementation with L-histidine during dietary zinc repletion improves short-term memory in zinc-restricted young adult male rats. J Nutr. 2000 Jun;130(6):1633-40. PMID: 10827222
332: Wang F, Zhao F, Guo J, Jing N. [Mechanism of impairment to microtubule polymerization resulting from zinc deficiency during pregnancy and lactation in mice] Wei Sheng Yan Jiu. 2000 May 30;29(3):156-8. Chinese. PMID: 12725061
333: King JC. Determinants of maternal zinc status during pregnancy. Am J Clin Nutr. 2000 May;71(5 Suppl):1334S-43S. Review. PMID: 10799411
334: Goto T, Komai M, Bryant BP, Furukawa Y. Reduction in carbonic anhydrase activity in the tongue epithelium and submandibular gland in zinc-deficient rats. Int J Vitam Nutr Res. 2000 May;70(3):110-8. PMID: 10883404
335: Wapnir RA. Zinc deficiency, malnutrition and the gastrointestinal tract. J Nutr. 2000 May;130(5S Suppl):1388S-92S. Review. PMID: 10801949
336: Fraker PJ, King LE, Laakko T, Vollmer TL. The dynamic link between the integrity of the immune system and zinc status. J Nutr. 2000 May;130(5S Suppl):1399S-406S. Review. PMID: 10801951
337: Scott ME, Koski KG. Zinc deficiency impairs immune responses against parasitic nematode infections at intestinal and systemic sites. J Nutr. 2000 May;130(5S Suppl):1412S-20S. Review. PMID: 10801953
338: Hambidge M. Human zinc deficiency. J Nutr. 2000 May;130(5S Suppl):1344S-9S. Review. PMID: 10801941
339: Shay NF, Mangian HF. Neurobiology of zinc-influenced eating behavior. J Nutr. 2000 May;130(5S Suppl):1493S-9S. Review. PMID: 10801965
340: Giralt M, Molinero A, Carrasco J, Hidalgo J. Effect of dietary zinc deficiency on brain metallothionein-I and -III mRNA levels during stress and inflammation. Neurochem Int. 2000 May;36(6):555-62. PMID: 10762093
341: Jankowski-Hennig MA, Clegg MS, Daston GP, Rogers JM, Keen CL. Zinc-deficient rat embryos have increased caspase 3-like activity and apoptosis. Biochem Biophys Res Commun. 2000 Apr 29;271(1):250-6. PMID: 10777711
342: Oteiza PI, Clegg MS, Zago MP, Keen CL. Zinc deficiency induces oxidative stress and AP-1 activation in 3T3 cells. Free Radic Biol Med. 2000 Apr 1;28(7):1091-9. PMID: 10832070
343: Coyle P, Philcox JC, Rofe AM. Zn-depleted mice absorb more of an intragastric Zn solution by a metallothionein-enhanced process than do Zn-replete mice. J Nutr. 2000 Apr;130(4):835-42. PMID: 10736338
344: Takeda A, Takefuta S, Okada S, Oku N. Relationship between brain zinc and transient learning impairment of adult rats fed zinc-deficient diet. Brain Res. 2000 Mar 24;859(2):352-7. PMID: 10719084
345: Sandstead HH. Causes of iron and zinc deficiencies and their effects on brain. J Nutr. 2000 Feb;130(2S Suppl):347S-349S. Review. PMID: 10721903
346: Meerarani P, Ramadass P, Toborek M, Bauer HC, Bauer H, Hennig B. Zinc protects against apoptosis of endothelial cells induced by linoleic acid and tumor necrosis factor alpha. Am J Clin Nutr. 2000 Jan;71(1):81-7. PMID: 10617950
347: Komai M, Goto T, Suzuki H, Takeda T, Furukawa Y. Zinc deficiency and taste dysfunction; contribution of carbonic anhydrase, a zinc-metalloenzyme, to normal taste sensation. Biofactors. 2000;12(1-4):65-70. PMID: 11216508
348: Kreft B, Fischer A, Kruger S, Sack K, Kirchner H, Rink L. The impaired immune response to diphtheria vaccination in elderly chronic hemodialysis patients is related to zinc deficiency. Biogerontology. 2000;1(1):61-6. PMID: 11707922
349: Fabe JS, Grahn BH, Paterson PG. Zinc concentration of selected ocular tissues in zinc-deficient rats. Biol Trace Elem Res. 2000 Summer;75(1-3):43-52. PMID: 11051595
350: Kudo H, Doi Y, Nishino T, Nara S, Hamasaki K, Fujimoto S. Dietary zinc deficiency decreases glutathione S-transferase expression in the rat olfactory epithelium. J Nutr. 2000 Jan;130(1):38-44. PMID: 10613764
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351: Cui L, Takagi Y, Sando K, Wasa M, Okada A. Nitric oxide synthase inhibitor attenuates inflammatory lesions in the skin of zinc-deficient rats. Nutrition. 2000 Jan;16(1):34-41. PMID: 10674233
352: Golub MS, Keen CL, Gershwin ME. Behavioral and hematologic consequences of marginal iron-zinc nutrition in adolescent monkeys and the effect of a powdered beef supplement. Am J Clin Nutr. 1999 Dec;70(6):1059-68. Erratum in: Am J Clin Nutr 2002 Mar;75(3):601. PMID: 10584051
353: Ozkan S, Ozkan H, Fetil E, Corapcioglu F, Yilmaz S, Ozer E. Acrodermatitis enteropathica with Pseudomonas aeruginosa sepsis. Pediatr Dermatol. 1999 Nov-Dec;16(6):444-7. PMID: 10632941
354: Kim SH, Keen CL. Influence of dietary carbohydrate on zinc-deficiency-induced changes in oxidative defense mechanisms and tissue oxidative damage in rats. Biol Trace Elem Res. 1999 Oct;70(1):81-96. PMID: 10493186
355: Reaves SK, Fanzo JC, Wu JY, Wang YR, Wu YW, Zhu L, Lei KY. Plasma apolipoprotein B-48, hepatic apolipoprotein B mRNA editing and apolipoprotein B mRNA editing catalytic subunit-1 mRNA levels are altered in zinc-deficient rats. J Nutr. 1999 Oct;129(10):1855-61. PMID: 10498758
356: Wauben IP, Xing HC, Wainwright PE. Neonatal dietary zinc deficiency in artificially reared rat pups retards behavioral development and interacts with essential fatty acid deficiency to alter liver and brain fatty acid composition. J Nutr. 1999 Oct;129(10):1773-81. PMID: 10498747
357: Stefanini M. Cutaneous bleeding related to zinc deficiency in two cases of advanced cancer. Cancer. 1999 Sep 1;86(5):866-70. PMID: 10463987
358: Worwag M, Classen HG, Schumacher E. Prevalence of magnesium and zinc deficiencies in nursing home residents in Germany. Magnes Res. 1999 Sep;12(3):181-9. PMID: 10488474
359: Fong LY, Magee PN. Dietary zinc deficiency enhances esophageal cell proliferation and N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumor incidence in C57BL/6 mouse. Cancer Lett. 1999 Aug 23;143(1):63-9. PMID: 10465339
360: Rojas AI, Phillips TJ. Patients with chronic leg ulcers show diminished levels of vitamins A and E, carotenes, and zinc. Dermatol Surg. 1999 Aug;25(8):601-4. PMID: 10491041
361: Ojima K, Ogura K, Sato T, Niwa M. Microvascular cast specimen formation of lingual papillae in zinc-deficient rat tongue. Anat Anz. 1999 Jul;181(4):371-5. PMID: 10427375
362: Ganapathy S, Volpe SL. Zinc, exercise, and thyroid hormone function. Crit Rev Food Sci Nutr. 1999 Jul;39(4):369-90. Review. PMID: 10442272
363: Eberle J, Schmidmayer S, Erben RG, Stangassinger M, Roth HP. Skeletal effects of zinc deficiency in growing rats. J Trace Elem Med Biol. 1999 Jul;13(1-2):21-6. PMID: 10445214
364: Abbasi A, Shetty K. [Zinc: pathophysiological effects, deficiency status and effects of supplementation in elderly persons--an overview of the research] Z Gerontol Geriatr. 1999 Jul;32 Suppl 1:I75-9. Review. German. PMID: 10441807
365: Van Loan MD, Sutherland B, Lowe NM, Turnlund JR, King JC. The effects of zinc depletion on peak force and total work of knee and shoulder extensor and flexor muscles. Int J Sport Nutr. 1999 Jun;9(2):125-35. PMID: 10362450
366: Miceli MV, Tate DJ Jr, Alcock NW, Newsome DA. Zinc deficiency and oxidative stress in the retina of pigmented rats. Invest Ophthalmol Vis Sci. 1999 May;40(6):1238-44. PMID: 10235558
367: Bucci I, Napolitano G, Giuliani C, Lio S, Minnucci A, Di Giacomo F, Calabrese G, Sabatino G, Palka G, Monaco F. Zinc sulfate supplementation improves thyroid function in hypozincemic Down children. Biol Trace Elem Res. 1999 Mar;67(3):257-68. PMID: 10201332
368: Forsleff L, Schauss AG, Bier ID, Stuart S. Evidence of functional zinc deficiency in Parkinson's disease. J Altern Complement Med. 1999 Feb;5(1):57-64. PMID: 10100031
369: Ruz M, Codoceo J, Galgani J, Munoz L, Gras N, Muzzo S, Leiva L, Bosco C. Single and multiple selenium-zinc-iodine deficiencies affect rat thyroid metabolism and ultrastructure. J Nutr. 1999 Jan;129(1):174-80. PMID: 9915896
370: Gross R, Hansel H, Schultink W, Shrimpton R, Matulessi P, Gross G, Tagliaferri E, Sastroamdijojo S. Moderate zinc and vitamin A deficiency in breast milk of mothers from East-Jakarta. Eur J Clin Nutr. 1998 Dec;52(12):884-90. PMID: 9881883
371: Gross R, Hansel H, Schultink W, Shrimpton R, Matulessi P, Gross G, Tagliaferri E, Sastroamdijojo S. Moderate zinc and vitamin A deficiency in breast milk of mothers from East-Jakarta. Eur J Clin Nutr. 1998 Dec;52(12):884-90. PMID: 9881883
372: Prasad AS. Zinc deficiency in humans: a neglected problem. J Am Coll Nutr. 1998 Dec;17(6):542-3. No abstract available. PMID: 9853531
373: Myung SJ, Yang SK, Jung HY, Jung SA, Kang GH, Ha HK, Hong WS, Min YI. Zinc deficiency manifested by dermatitis and visual dysfunction in a patient with Crohn's disease. J Gastroenterol. 1998 Dec;33(6):876-9. PMID: 9853564
374: Rains TM, Hedrick S, Randall AC, Lee RG, Kennedy KJ, Shay NF. Food intake patterns are altered during long-term zinc deficiency in rats. Physiol Behav. 1998 Dec 1;65(3):473-8. PMID: 9877413
375: Ninh NX, Maiter D, Verniers J, Lause P, Ketelslegers JM, Thissen JP. Failure of exogenous IGF-I to restore normal growth in rats submitted to dietary zinc deprivation. J Endocrinol. 1998 Nov;159(2):211-7. PMID: 9795360
376: Chen SM, Young TK. Effects of zinc deficiency on endogenous antioxidant enzymes and lipid peroxidation in glomerular cells of normal and five-sixths nephrectomized rats. J Formos Med Assoc. 1998 Nov;97(11):750-6. PMID: 9872031
377: Cha MC, Rojhani A. Failure of IGF-I infusion to promote growth in Zn deficient hypophysectomized rats. J Trace Elem Med Biol. 1998 Nov;12(3):141-7. PMID: 9857326
378: Ripa S, Ripa R, Giustiniani S. Are failured cardiomyopathies a zinc-deficit related disease? A study on Zn and Cu in patients with chronic failured dilated and hypertrophic cardiomyopathies. Minerva Med. 1998 Nov-Dec;89(11-12):397-403. PMID: 10212663
379: Prasad AS. Zinc and immunity. Mol Cell Biochem. 1998 Nov;188(1-2):63-9. Review. PMID: 9823012
380: Kleier C, Werkmeister R, Joos U. [Zinc and vitamin A deficiency in diseases of the mouth mucosa] Mund Kiefer Gesichtschir. 1998 Nov;2(6):320-5. German. PMID: 9881002
381: Adisa AO, Odutuga AA. Changes in the activities of three diagnostic enzymes in the heart of rats following the consumption of diets deficient in zinc and essential fatty acids. Biochem Mol Biol Int. 1998 Oct;46(3):571-6. PMID: 9818096
382: Yanagisawa H, Nodera M, Wada O. Zinc deficiency aggravates tubulointerstitial nephropathy caused by ureteral obstruction. Biol Trace Elem Res. 1998 Oct;65(1):1-6. PMID: 9877532
383: MacDonald RS, Wollard-Biddle LC, Browning JD, Thornton WH Jr, O'Dell BL. Zinc deprivation of murine 3T3 cells by use of diethylenetrinitrilopentaacetate impairs DNA synthesis upon stimulation with insulin-like growth factor-1 (IGF-1). J Nutr. 1998 Oct;128(10):1600-5. PMID: 9772124
384: Thornton WH Jr, MacDonald RS, Wollard-Biddle LC, Browning JD, O'Dell BL. Chelation of extracellular zinc inhibits proliferation in 3T3 cells independent of insulin-like growth factor-I receptor expression. Proc Soc Exp Biol Med. 1998 Oct;219(1):64-8. PMID: 9751224
385: Okegbile EO, Odunuga O, Oyewo A. Effect of dietary zinc deficiency on alkaline phosphatase and nucleic acids in rats. Afr J Med Med Sci. 1998 Sep-Dec;27(3-4):189-92. PMID: 10497646
386: Caulfield LE, Zavaleta N, Shankar AH, Merialdi M. Potential contribution of maternal zinc supplementation during pregnancy to maternal and child survival. Am J Clin Nutr. 1998 Aug;68(2 Suppl):499S-508S. Review. PMID: 9701168
387: Ruel MT, Bouis HE. Plant breeding: a long-term strategy for the control of zinc deficiency in vulnerable populations. Am J Clin Nutr. 1998 Aug;68(2 Suppl):488S-494S. Review. PMID: 9701166
388: Gibson RS, Yeudall F, Drost N, Mtitimuni B, Cullinan T. Dietary interventions to prevent zinc deficiency. Am J Clin Nutr. 1998 Aug;68(2 Suppl):484S-487S. Review. PMID: 9701165
389: Black MM. Zinc deficiency and child development. Am J Clin Nutr. 1998 Aug;68(2 Suppl):464S-469S. Review. PMID: 9701161
390: Marchetti P, Amodio P, Caregaro L, Gatta A. [Zinc deficiency in liver cirrhosis: a curiosity or a problem?] Ann Ital Med Int. 1998 Jul-Sep;13(3):157-62. Review. Italian. PMID: 9859572
391: Cui L, Takagi Y, Wasa M, Iiboshi Y, Inoue M, Khan J, Sando K, Nezu R, Okada A. Zinc deficiency enhances interleukin-1alpha-induced metallothionein-1 expression in rats. J Nutr. 1998 Jul;128(7):1092-8. PMID: 9649590
392: Lee RG, Rains TM, Tovar-Palacio C, Beverly JL, Shay NF. Zinc deficiency increases hypothalamic neuropeptide Y and neuropeptide Y mRNA levels and does not block neuropeptide Y-induced feeding in rats. J Nutr. 1998 Jul;128(7):1218-23. PMID: 9649609
393: Obladen M, Loui A, Kampmann W, Renz H. Zinc deficiency in rapidly growing preterm infants. Acta Paediatr. 1998 Jun;87(6):685-91. PMID: 9686664
394: Persson LA, Lundstrom M, Lonnerdal B, Hernell O. Are weaning foods causing impaired iron and zinc status in 1-year-old Swedish infants? A cohort study. Acta Paediatr. 1998 Jun;87(6):618-22. PMID: 9686651
395: Doerr TD, Marks SC, Shamsa FH, Mathog RH, Prasad AS. Effects of zinc and nutritional status on clinical outcomes in head and neck cancer. Nutrition. 1998 Jun;14(6):489-95. PMID: 9646288
396: Osati-Ashtiani F, King LE, Fraker PJ. Variance in the resistance of murine early bone marrow B cells to a deficiency in zinc. Immunology. 1998 May;94(1):94-100. PMID: 9708192
397: Naber TH, van den Hamer CJ, Baadenhuysen H, Jansen JB. The value of methods to determine zinc deficiency in patients with Crohn's disease. Scand J Gastroenterol. 1998 May;33(5):514-23. PMID: 9648992
398: Gibson RS, Huddle JM. Suboptimal zinc status in pregnant Malawian women: its association with low intakes of poorly available zinc, frequent reproductive cycling, and malaria. Am J Clin Nutr. 1998 Apr;67(4):702-9. PMID: 9537617
399: Piela Z, Szuber M, Mach B, Janniger CK. Zinc deficiency in exclusively breast-fed infants. Cutis. 1998 Apr;61(4):197-200. PMID: 9564591
400: Huddle JM, Gibson RS, Cullinan TR. Is zinc a limiting nutrient in the diets of rural pregnant Malawian women? Br J Nutr. 1998 Mar;79(3):257-65. PMID: 9577304
401: Rosado JL. [Zinc deficiency and its functional implications] Salud Publica Mex. 1998 Mar-Apr;40(2):181-8. Review. Spanish. PMID: 9617199
402: Kim ES, Noh SK, Koo SI. Marginal zinc deficiency lowers the lymphatic absorption of alpha-tocopherol in rats. J Nutr. 1998 Feb;128(2):265-70. PMID: 9446854
403: Stevens J, Lubitz L. Symptomatic zinc deficiency in breast-fed term and premature infants. J Paediatr Child Health. 1998 Feb;34(1):97-100. PMID: 9568953
404: Kilic I, Ozalp I, Coskun T, Tokatli A, Emre S, Saldamli I, Koksel H, Ozboy O. The effect of zinc-supplemented bread consumption on school children with asymptomatic zinc deficiency. J Pediatr Gastroenterol Nutr. 1998 Feb;26(2):167-71. PMID: 9481631
405: Li J, Xu P, He Z. [Effect of zinc deficiency on apoptosis of spermatogenic cells of rat tostis] Zhonghua Yi Xue Za Zhi. 1998 Feb;78(2):91-3. Chinese. PMID: 10923414
406: Clausen T, Dorup I. Micronutrients, minerals and growth control. Bibl Nutr Dieta. 1998;(54):84-92. Review. PMID: 9597174
407: Wang P, Yang Z. [Influence of insufficient zinc on immune functions in NIDDM patients] Hunan Yi Ke Da Xue Xue Bao. 1998;23(6):599-601. Chinese. PMID: 10806782
408: Shi HN, Scott ME, Stevenson MM, Koski KG. Energy restriction and zinc deficiency impair the functions of murine T cells and antigen-presenting cells during gastrointestinal nematode infection. J Nutr. 1998 Jan;128(1):20-7. PMID: 9430597
409: Kennedy KJ, Rains TM, Shay NF. Zinc deficiency changes preferred macronutrient intake in subpopulations of Sprague-Dawley outbred rats and reduces hepatic pyruvate kinase gene expression. J Nutr. 1998 Jan;128(1):43-9. PMID: 9430600
410: Browning JD, MacDonald RS, Thornton WH, O'Dell BL. Reduced food intake in zinc deficient rats is normalized by megestrol acetate but not by insulin-like growth factor-I. J Nutr. 1998 Jan;128(1):136-42. PMID: 9430615
411: Inoue K, Kito M, Kato S, Osawa M, Okuda H, Yabuta K, Maeda T. A case of acquired zinc deficiency in a mature breast-fed infant. J Perinat Med. 1998;26(6):495-7. PMID: 10224609
412: Solomons NW. Mild human zinc deficiency produces an imbalance between cell-mediated and humoral immunity. Nutr Rev. 1998 Jan;56(1 Pt 1):27-8. Review. PMID: 9481116
413: Watanabe T, Endo A. Cytogenetic effects of cadmium on unfertilized oocytes in short-term zinc deficiency in hamsters. Mutat Res. 1997 Dec 12;395(2-3):113-8. PMID: 9465921
414: Stone J, Doube A, Dudson D, Wallace J. Inadequate calcium, folic acid, vitamin E, zinc, and selenium intake in rheumatoid arthritis patients: results of a dietary survey. Semin Arthritis Rheum. 1997 Dec;27(3):180-5. PMID: 9431590
415: Ray SK, Roychoudhury R, Bandopadhyay SK, Basu S. Studies on 'zinc deficiency syndrome' in black bengal goats (Capra hircus) fed with fodder (Andropogon gayanus) grown on soil treated with an excess of calcium and phosphorus fertilizer. Vet Res Commun. 1997 Nov;21(8):541-6. PMID: 9444077
416: Zorbas YG, Yaroshenko YN, Kuznetsov NK, Ivanov AL. Daily zinc supplementation effect on zinc deficiency in rats during prolonged restriction of motor activity. Biol Trace Elem Res. 1997 Oct-Nov;60(1-2):101-13. PMID: 9404679
417: Doerr TD, Prasad AS, Marks SC, Beck FW, Shamsa FH, Penny HS, Mathog RH. Zinc deficiency in head and neck cancer patients. J Am Coll Nutr. 1997 Oct;16(5):418-22. PMID: 9322189
418: Kong X, Ren R, Liu L. [Effects of zinc deficiency in fodder on brain development, learning and memory in rats] Zhonghua Yu Fang Yi Xue Za Zhi. 1997 Sep;31(5):295-8. Chinese. PMID: 9812610
419: Fong LY, Lau KM, Huebner K, Magee PN. Induction of esophageal tumors in zinc-deficient rats by single low doses of N-nitrosomethylbenzylamine (NMBA): analysis of cell proliferation, and mutations in H-ras and p53 genes. Carcinogenesis. 1997 Aug;18(8):1477-84. PMID: 9276619
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424: Dorea JG. Zinc in urban infants and children from Brasilia. Arch Latinoam Nutr. 1997 Jun;47(2 Suppl 1):39-40. PMID: 9659417
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427: Hamdi SA, Nassif OI, Ardawi MS. Effect of marginal or severe dietary zinc deficiency on testicular development and functions of the rat. Arch Androl. 1997 May-Jun;38(3):243-53. PMID: 9140621
428: Humphrey PA, Ashraf M, Lee CM. Hepatic cells' mitotic and peritoneal macrophage phagocytic activities during Trypanosoma musculi infection in zinc-deficient mice. J Natl Med Assoc. 1997 Apr;89(4):259-67. PMID: 9145631
429: Gupta RP, Verma PC, Garg SL. Effect of experimental zinc deficiency on thyroid gland in guinea-pigs. Ann Nutr Metab. 1997;41(6):376-81. PMID: 9491194
430: Cha MC, Rojhani A. Zinc deficiency inhibits the direct growth effect of growth hormone on the tibia of hypophysectomized rats. Biol Trace Elem Res. 1997 Winter;59(1-3):99-111. PMID: 9522052
431: DiSilvestro RA, Blostein-Fujii A. Moderate zinc deficiency in rats enhances lipoprotein oxidation in vitro. Free Radic Biol Med. 1997;22(4):739-42. PMID: 9013138
432: Selvais PL, Labuche C, Nguyen XN, Ketelslegers JM, Denef JF, Maiter DM. Cyclic feeding behaviour and changes in hypothalamic galanin and neuropeptide Y gene expression induced by zinc deficiency in the rat. J Neuroendocrinol. 1997 Jan;9(1):55-62. PMID: 9023738
433: Newberne PM, Broitman S, Schrager TF. Esophageal carcinogenesis in the rat: zinc deficiency, DNA methylation and alkyltransferase activity. Pathobiology. 1997;65(5):253-63. PMID: 9459495
434: Newberne PM, Schrager TF, Broitman S. Esophageal carcinogenesis in the rat: zinc deficiency and alcohol effects on tumor induction. Pathobiology. 1997;65(1):39-45. PMID: 9200188
435: Prasad AS, Beck FW, Grabowski SM, Kaplan J, Mathog RH. Zinc deficiency: changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and in noncancer subjects. Proc Assoc Am Physicians. 1997 Jan;109(1):68-77. PMID: 9010918
436: Golub MS, Takeuchi PT, Keen CL, Hendrickx AG, Gershwin ME. Activity and attention in zinc-deprived adolescent monkeys. Am J Clin Nutr. 1996 Dec;64(6):908-15. PMID: 8942416
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438: Terril-Robb LA, Clemons DJ, Besch-Williford C, O'Brien DP, O'Dell BL. Morphophysiologic characterization of peripheral neuropathy in zinc-deficient guinea pigs. Proc Soc Exp Biol Med. 1996 Oct;213(1):50-8. PMID: 8820823
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440: Fong LY, Li JX, Farber JL, Magee PN. Cell proliferation and esophageal carcinogenesis in the zinc-deficient rat. Carcinogenesis. 1996 Sep;17(9):1841-8. PMID: 8824504
441: Fan PC, Teng RJ, Chou CC, Wu TJ, Tsou Yau KI, Hsieh KH. Impaired immune function in a premature infant with zinc deficiency after total parenteral nutrition. Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1996 Sep-Oct;37(5):364-9. PMID: 8942032
442: Eder K, Kirchgessner M. Zinc deficiency and the desaturation of linoleic acid in rats force-fed fat-free diets. Biol Trace Elem Res. 1996 Aug;54(2):173-83. PMID: 8886317
443: Haglund B, Ryckenberg K, Selinus O, Dahlquist G. Evidence of a relationship between childhood-onset type I diabetes and low groundwater concentration of zinc. Diabetes Care. 1996 Aug;19(8):873-5. PMID: 8842606
444: Mori H, Matsumoto Y, Tamada Y, Ohashi M. Apoptotic cell death in formation of vesicular skin lesions in patients with acquired zinc deficiency. J Cutan Pathol. 1996 Aug;23(4):359-63. PMID: 8864924
445: Molina EL, Patel JA. A to Z: vitamin A and zinc, the miracle duo. Indian J Pediatr. 1996 Jul-Aug;63(4):427-31. Review. PMID: 10832460
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447: Prasad AS, Beck FW, Endre L, Handschu W, Kukuruga M, Kumar G. Zinc deficiency affects cell cycle and deoxythymidine kinase gene expression in HUT-78 cells. J Lab Clin Med. 1996 Jul;128(1):51-60. PMID: 8759936
448: Pescovitz MD, Mehta PL, Jindal RM, Milgrom ML, Leapman SB, Filo RS. Zinc deficiency and its repletion following liver transplantation in humans. Clin Transplant. 1996 Jun;10(3):256-60. PMID: 8826662
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450: Kremer JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol. 1996 Jun;23(6):990-4. PMID: 8782128
451: Naber TH, Baadenhuysen H, Jansen JB, van den Hamer CJ, van den Broek W. Serum alkaline phosphatase activity during zinc deficiency and long-term inflammatory stress. Clin Chim Acta. 1996 May 30;249(1-2):109-27. PMID: 8737596
452: Kralik A, Eder K, Kirchgessner M. Influence of zinc and selenium deficiency on parameters relating to thyroid hormone metabolism. Horm Metab Res. 1996 May;28(5):223-6. PMID: 8738110
453: Papadopoulou A, Nathavitharana K, Williams MD, Darbyshire PJ, Booth IW. Diagnosis and clinical associations of zinc depletion following bone marrow transplantation. Arch Dis Child. 1996 Apr;74(4):328-31. PMID: 8669934
454: Ojuawo A, Lindley KJ, Milla PJ. Serum zinc, selenium and copper concentration in children with allergic colitis. East Afr Med J. 1996 Apr;73(4):236-8. PMID: 8706606
455: Prasad AS. Zinc deficiency in women, infants and children. J Am Coll Nutr. 1996 Apr;15(2):113-20. Review. PMID: 8778139
456: Om AS, Chung KW. Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver. J Nutr. 1996 Apr;126(4):842-8. PMID: 8613886
457: Bhandari N, Bahl R, Hambidge KM, Bhan MK. Increased diarrhoeal and respiratory morbidity in association with zinc deficiency--a preliminary report. Acta Paediatr. 1996 Feb;85(2):148-50. PMID: 8640039
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459: Ashrafi SH, Said-al-Naief NA. Zinc deficiency produces time-related ultrastructural changes in rat cheek epithelium. Scanning Microsc. 1996;10(1):209-17; discussion 217-8. PMID: 9813606
460: Khedun SM, Naicker T, Maharaj B. Zinc, hydrochlorothiazide and sexual dysfunction. Cent Afr J Med. 1995 Oct;41(10):312-5. PMID: 8556776
461: Ripa S, Ripa R. [Zinc and diabetes mellitus] Minerva Med. 1995 Oct;86(10):415-21. Review. Italian. PMID: 8622809
462: Cunnane SC, Yang J. Zinc deficiency impairs whole-body accumulation of polyunsaturates and increases the utilization of [1-14C]linoleate for de novo lipid synthesis in pregnant rats. Can J Physiol Pharmacol. 1995 Sep;73(9):1246-52. PMID: 8748973
463: Rogers JM, Taubeneck MW, Daston GP, Sulik KK, Zucker RM, Elstein KH, Jankowski MA, Keen CL. Zinc deficiency causes apoptosis but not cell cycle alterations in organogenesis-stage rat embryos: effect of varying duration of deficiency. Teratology. 1995 Sep;52(3):149-59. PMID: 8638255
464: Said al-Naief NA, Ashrafi SH. Time-related changes induced by zinc-deficient diet in the concentration of rat cheek epithelial membrane-coating granules. Arch Oral Biol. 1995 Aug;40(8):717-22. PMID: 7487572
465: Eder K, Kirchgessner M. Activities of liver microsomal fatty acid desaturases in zinc-deficient rats force-fed diets with a coconut oil/safflower oil mixture of linseed oil. Biol Trace Elem Res. 1995 Jun;48(3):215-29. PMID: 9398942
466: Watanabe T, Arakawa T, Fukuda T, Higuchi K, Kobayashi K. Zinc deficiency delays gastric ulcer healing in rats. Dig Dis Sci. 1995 Jun;40(6):1340-4. PMID: 7781457
467: Ripa S, Ripa R. Zinc and the elderly. Minerva Med. 1995 Jun;86(6):275-8. Review. PMID: 7566561
468: Ghassemifar MR, Olsson MG, Agren MS, Franzen LE. Impaired function of postoperative macrophages from zinc-deficient rats decreases collagen contraction. Brief report. APMIS. 1995 May;103(5):395-400. PMID: 7654364
469: Braga-Costa TM, De-Oliveira LM, Vannucchi H. Effect of zinc deficiency induced before and during pregnancy on the survival of female rats and their pups. Braz J Med Biol Res. 1995 May;28(5):569-74. PMID: 8555977
470: King LE, Osati-Ashtiani F, Fraker PJ. Depletion of cells of the B lineage in the bone marrow of zinc-deficient mice. Immunology. 1995 May;85(1):69-73. PMID: 7635524
471: Oteiza PI, Olin KL, Fraga CG, Keen CL. Zinc deficiency causes oxidative damage to proteins, lipids and DNA in rat testes. J Nutr. 1995 Apr;125(4):823-9. PMID: 7722683
472: McNall AD, Etherton TD, Fosmire GJ. The impaired growth induced by zinc deficiency in rats is associated with decreased expression of the hepatic insulin-like growth factor I and growth hormone receptor genes. J Nutr. 1995 Apr;125(4):874-9. PMID: 7722689
473: Ninh NX, Thissen JP, Maiter D, Adam E, Mulumba N, Ketelslegers JM. Reduced liver insulin-like growth factor-I gene expression in young zinc-deprived rats is associated with a decrease in liver growth hormone (GH) receptors and serum GH-binding protein. J Endocrinol. 1995 Mar;144(3):449-56. PMID: 7738469
474: Jankowski MA, Uriu-Hare JY, Rucker RB, Rogers JM, Keen CL. Maternal zinc deficiency, but not copper deficiency or diabetes, results in increased embryonic cell death in the rat: implications for mechanisms underlying abnormal development. Teratology. 1995 Feb;51(2):85-93. PMID: 7660326
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476: Stiles NJ, Boosalis MG. Case report of zinc deficiency in an elderly woman. Clin Lab Sci. 1995 Jan-Feb;8(1):39-42. PMID: 10150466
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479: Prasad AS. Zinc: an overview. Nutrition. 1995 Jan-Feb;11(1 Suppl):93-9. Review. PMID: 7749260
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481: Sole D, Rieckmann B, Lippelt RM, Lippelt RT, Amancio OM, Queiroz Sde S, Naspitz CK. Zinc deficient diet consequences for pregnancy and offsprings of Wistar rats. Rev Paul Med. 1995 Jan-Feb;113(1):681-6. PMID: 8578076
482: Peters JM, Wiley LM, Zidenberg-Cherr S, Keen CL. Periconceptional zinc deficiency affects uterine 3H-estradiol binding in mice. Teratog Carcinog Mutagen. 1995;15(1):23-31. PMID: 7604389
483: Eder K, Kirchgessner M. Levels of polyunsaturated fatty acids in tissues from zinc-deficient rats fed a linseed oil diet. Lipids. 1994 Dec;29(12):839-44. PMID: 7854009
484: Ozturk G, Erbas D, Imir T, Bor NM. Decreased natural killer (NK) cell activity in zinc-deficient rats. Gen Pharmacol. 1994 Nov;25(7):1499-503. PMID: 7896066
485: Parsons SE, DiSilvestro RA. Effects of mild zinc deficiency, plus or minus an acute-phase response, on galactosamine-induced hepatitis in rats. Br J Nutr. 1994 Oct;72(4):611-8. PMID: 7986791
486: Yang J, Cunnane SC. Quantitative measurements of dietary and [1-14C]linoleate metabolism in pregnant rats: specific influence of moderate zinc depletion independent of food intake. Can J Physiol Pharmacol. 1994 Oct;72(10):1180-5. PMID: 7882183
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488: Sandstead HH. Understanding zinc: recent observations and interpretations. J Lab Clin Med. 1994 Sep;124(3):322-7. Review. PMID: 8083574
489: Menzano E, Carlen PL. Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunction--a review. Alcohol Clin Exp Res. 1994 Aug;18(4):895-901. Review. PMID: 7978102
490: Golub MS, Takeuchi PT, Keen CL, Gershwin ME, Hendrickx AG, Lonnerdal B. Modulation of behavioral performance of prepubertal monkeys by moderate dietary zinc deprivation. Am J Clin Nutr. 1994 Aug;60(2):238-43. PMID: 8030602
491: Humphrey PA, Lee CM, Ashraf M. Changes in immunoglobulin levels in zinc-deficient mice infected with Trypanosoma musculi. J Natl Med Assoc. 1994 Aug;86(8):613-9. PMID: 7932840
492: Shi HN, Scott ME, Stevenson MM, Koski KG. Zinc deficiency impairs T cell function in mice with primary infection of Heligmosomoides polygyrus (Nematoda). Parasite Immunol. 1994 Jul;16(7):339-50. PMID: 7970873
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494: Martin GB, White CL, Markey CM, Blackberry MA. Effects of dietary zinc deficiency on the reproductive system of young male sheep: testicular growth and the secretion of inhibin and testosterone. J Reprod Fertil. 1994 May;101(1):87-96. PMID: 8064696
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496: White CL, Martin GB, Hynd PI, Chapman RE. The effect of zinc deficiency on wool growth and skin and wool follicle histology of male Merino lambs. Br J Nutr. 1994 Mar;71(3):425-35. PMID: 8172871
497: Browning JD, O'Dell BL. Low zinc status in guinea pigs impairs calcium uptake by brain synaptosomes. J Nutr. 1994 Mar;124(3):436-43. PMID: 7907139
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504: Reeves PG, Rossow KL. Zinc deficiency affects the activity and protein concentration of angiotensin-converting enzyme in rat testes. Proc Soc Exp Biol Med. 1993 Jul;203(3):336-42. PMID: 8390691
505: Fushimi H, Inoue T, Yamada Y, Horie H, Kameyama M, Inoue K, Minami T, Okazaki Y. Zinc deficiency exaggerates diabetic osteoporosis. Diabetes Res Clin Pract. 1993 Jun;20(3):191-6. PMID: 8404452
506: Cook-Mills JM, Fraker PJ. Functional capacity of the residual lymphocytes from zinc-deficient adult mice. Br J Nutr. 1993 May;69(3):835-48. PMID: 8329358
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511: Shoji S, Miyamoto H, Nomoto S. Adverse effect of antipyretic agent on serum zinc. Ann Clin Lab Sci. 1993 Mar-Apr;23(2):106-10. PMID: 8457139
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515: Shay NF, Cousins RJ. Cloning of rat intestinal mRNAs affected by zinc deficiency. J Nutr. 1993 Jan;123(1):35-41. PMID: 8421228
516: Peters JM, Wiley LM, Zidenberg-Cherr S, Keen CL. Influence of periconceptional zinc deficiency on embryonic plasma membrane function in mice. Teratog Carcinog Mutagen. 1993;13(1):15-21. PMID: 8100649
517: Jendryczko A, Sodowska H, Drozdz M. [Zinc deficiency in children infected with Giardia lamblia] Wiad Lek. 1993 Jan-Feb;46(1-2):32-5. Polish. PMID: 8249376
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524: Taneja SK, Arya P. Influence of low dietary lipid content on anorexia and [14C]glucose uptake in the intestine of zinc-deficient mice. Br J Nutr. 1992 Sep;68(2):505-14. PMID: 1445829
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526: Barch DH, Fox CC, Rosche WA, Rundhaugen LM, Wrighton SA. Inhibition of rat methylbenzylnitrosamine metabolism by dietary zinc and zinc in vitro. Gastroenterology. 1992 Sep;103(3):800-6. PMID: 1499930
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528: Van Voorhees AS, Riba M. Acquired zinc deficiency in association with anorexia nervosa: case report and review of the literature. Pediatr Dermatol. 1992 Sep;9(3):268-71. Review. PMID: 1488378
529: Lukaski HC, Hall CB, Marchello MJ. Impaired thyroid hormone status and thermoregulation during cold exposure of zinc-deficient rats. Horm Metab Res. 1992 Aug;24(8):363-6. PMID: 1526622
530: Hunt CD, Johnson PE, Herbel J, Mullen LK. Effects of dietary zinc depletion on seminal volume and zinc loss, serum testosterone concentrations, and sperm morphology in young men. Am J Clin Nutr. 1992 Jul;56(1):148-57. PMID: 1609752
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535: Peck MD, Alexander JW. Interaction of protein and zinc malnutrition with the murine response to infection. JPEN J Parenter Enteral Nutr. 1992 May-Jun;16(3):232-5. PMID: 1501352
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538: Avery RA, Bettger WJ. Zinc deficiency alters the protein composition of the membrane skeleton but not the extractability or oligomeric form of spectrin in rat erythrocyte membranes. J Nutr. 1992 Mar;122(3):428-34. PMID: 1542001
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543: Mobarhan S, Greenberg B, Mehta R, Friedman H, Barch D. Zinc deficiency reduces hepatic cellular retinol-binding protein in rats. Int J Vitam Nutr Res. 1992;62(2):148-54. PMID: 1517037
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556: Constantinidis J. The hypothesis of zinc deficiency in the pathogenesis of neurofibrillary tangles. Med Hypotheses. 1991 Aug;35(4):319-23. PMID: 1943884
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558: Waalkes MP, Kovatch R, Rehm S. Effect of chronic dietary zinc deficiency on cadmium toxicity and carcinogenesis in the male Wistar [Hsd: (WI)BR] rat. Toxicol Appl Pharmacol. 1991 May;108(3):448-56. PMID: 2020969
559: Feller DJ, Tso-Olivas DY, Savage DD. Hippocampal mossy fiber zinc deficit in mice genetically selected for ethanol withdrawal seizure susceptibility. Brain Res. 1991 Apr 5;545(1-2):73-9. PMID: 1860062
560: Van der Rijt CC, Schalm SW, Schat H, Foeken K, De Jong G. Overt hepatic encephalopathy precipitated by zinc deficiency. Gastroenterology. 1991 Apr;100(4):1114-8. PMID: 2001810
561: Prasad AS. Discovery of human zinc deficiency and studies in an experimental human model. Am J Clin Nutr. 1991 Feb;53(2):403-12. Review. PMID: 1989405
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563: Apgar J, Everett GA. Low zinc intake affects maintenance of pregnancy in guinea pigs. J Nutr. 1991 Feb;121(2):192-200. PMID: 1847415
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568: Agren MS, Franzen L. Influence of zinc deficiency on breaking strength of 3-week-old skin incisions in the rat. Acta Chir Scand. 1990 Oct;156(10):667-70. PMID: 2264423
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576: Lofts RH, Schroeder SR, Maier RH. Effects of serum zinc supplementation on pica behavior of persons with mental retardation. Am J Ment Retard. 1990 Jul;95(1):103-9. PMID: 2386628
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580: Michaelsson G, Ljunghall K. Patients with dermatitis herpetiformis, acne, psoriasis and Darier's disease have low epidermal zinc concentrations. Acta Derm Venereol. 1990;70(4):304-8. PMID: 1977254
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586: Browning JD, O'Dell BL. Zinc deficiency decreases the concentration of N-methyl-D-aspartate receptors in guinea pig cortical synaptic membranes. J Nutr. 1995 Aug;125(8):2083-9. PMID: 7643242
587: Kaswan S, Bedwal RS. Light and electron microscopic changes in the ovary of zinc deficient BALB/c mice. Indian J Exp Biol. 1995 Jul;33(7):469-79. PMID: 7590954
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602: Canton MC, Cotter BM, Cremin FM, Morrissey PA. The effect of dietary zinc deficiency on pancreatic gamma-glutamyl hydrolase (EC 3.4.22.12) activity and on the absorption of pteroylpolyglutamate in rats. Br J Nutr. 1989 Jul;62(1):185-93. PMID: 2789981
603: Gibson RS, Vanderkooy PD, MacDonald AC, Goldman A, Ryan BA, Berry M. A growth-limiting, mild zinc-deficiency syndrome in some southern Ontario boys with low height percentiles. Am J Clin Nutr. 1989 Jun;49(6):1266-73. PMID: 2729165
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617: Southon S, Kechrid Z, Wright AJ, Fairweather-Tait SJ. Effect of reduced dietary zinc intake on carbohydrate and Zn metabolism in the genetically diabetic mouse (C57BL/KsJ db+/db+). Br J Nutr. 1988 Nov;60(3):499-507. PMID: 3219321
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622: Avery RA, Bettger WJ. Effect of dietary zinc deficiency and the associated drop in voluntary food intake on rat erythrocyte membrane polyamines. J Nutr. 1988 Aug;118(8):987-94. PMID: 3404290
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626: Gupta RP, Verma PC, Sadana JR, Gupta RK. Studies on the pathology of experimental zinc deficiency in guinea-pigs. J Comp Pathol. 1988 May;98(4):405-13. PMID: 3417909
627: Vruwink KG, Hurley LS, Gershwin ME, Keen CL. Gestational zinc deficiency amplifies the regulation of metallothionein induction in adult mice. Proc Soc Exp Biol Med. 1988 May;188(1):30-4. PMID: 3368476
628: Pinelli A, Trivulzio S. Antiprostatic effect associated with zinc depletion in cimetidine-treated rats. Pharmacol Res Commun. 1988 Apr;20(4):329-35. PMID: 3387461
629: De Virgiliis S, Congia M, Turco MP, Frau F, Dessi C, Argiolu F, Sorcinelli R, Sitzia A, Cao A. Depletion of trace elements and acute ocular toxicity induced by desferrioxamine in patients with thalassaemia. Arch Dis Child. 1988 Mar;63(3):250-5. PMID: 3355204
630: Babenko GA, Zaviiskii IuM. [Effect of exogenous zinc deficiency on the duration of skin graft functioning] Vopr Pitan. 1988 Mar-Apr;(2):48-51. Russian. PMID: 3291391
631: Glover MT, Atherton DJ. Transient zinc deficiency in two full-term breast-fed siblings associated with low maternal breast milk zinc concentration. Pediatr Dermatol. 1988 Feb;5(1):10-3. PMID: 3380757
632: Suliman HB, Abdelrahim AI, Zakia AM, Shommein AM. Zinc deficiency in sheep: field cases. Trop Anim Health Prod. 1988 Feb;20(1):47-51. PMID: 3354059
633: Koo SI, Lee CC. Compositional changes in plasma high-density lipoprotein particles in marginally zinc-deficient male rats. Am J Clin Nutr. 1988 Jan;47(1):120-7. PMID: 3337030
634: Chen SY. Studies on cell migration, adenylate cyclase and membrane-coating granules in the buccal epithelium of the zinc-deficient rabbit, including the influence of isoproterenol. Arch Oral Biol. 1988;33(9):645-51. PMID: 3245789
635: Naganuma M, Ikeda M, Tomita H. Changes in soft palate taste buds of rats due to aging and zinc deficiency--scanning electron microscopic observation. Auris Nasus Larynx. 1988;15(2):117-27. PMID: 3207412
636: Verma PC, Gupta RP, Sadana JR, Gupta RK. Effect of experimental zinc deficiency and repletion on some immunological variables in guinea-pigs. Br J Nutr. 1988 Jan;59(1):149-54. PMID: 2449907
637: Harding AJ, Dreosti IE, Tulsi RS. Zinc deficiency in the 11 day rat embryo: a scanning and transmission electron microscope study. Life Sci. 1988;42(8):889-96. PMID: 3343888
638: Cannon DS, Crawford IL, Carrell LE. Zinc deficiency conditions food aversions in rats. Physiol Behav. 1988;42(3):245-7. PMID: 3406151
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645: Milne DB, Canfield WK, Gallagher SK, Hunt JR, Klevay LM. Ethanol metabolism in postmenopausal women fed a diet marginal in zinc. Am J Clin Nutr. 1987 Oct;46(4):688-93. PMID: 3661484
646: Barch DH, Fox CC. Dietary zinc deficiency increases the methylbenzylnitrosamine-induced formation of O6-methylguanine in the esophageal DNA of the rat. Carcinogenesis. 1987 Oct;8(10):1461-4. PMID: 3652382
647: Favier M, Favier A, Robert E, Guignier M, Malinas Y. [Can zinc deficiency in the mother be responsible for the occurrence of spina bifida aperta in the fetus?] Rev Fr Gynecol Obstet. 1987 Oct;82(10):575-81. French. PMID: 2446372
648: Katz RL, Keen CL, Litt IF, Hurley LS, Kellams-Harrison KM, Glader LJ. Zinc deficiency in anorexia nervosa. J Adolesc Health Care. 1987 Sep;8(5):400-6. PMID: 3312133
649: Morrison JN, Bremner I. Effect of maternal zinc supply on blood and tissue metallothionein I concentrations in suckling rats. J Nutr. 1987 Sep;117(9):1588-94. PMID: 3655938
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657: Browning JD, Reeves PG, O'Dell BL. Zinc deficiency in rats reduces the vasodilation response to bradykinin and prostacyclin. J Nutr. 1987 Mar;117(3):490-5. PMID: 2883270
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670: Jacobson SG, Meadows NJ, Keeling PW, Mitchell WD, Thompson RP. Rod mediated retinal dysfunction in cats with zinc depletion: comparison with taurine depletion. Clin Sci (Lond). 1986 Nov;71(5):559-64. PMID: 3769404
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673: Kawamoto JC, Castonguay TW, Keen CL, Stern JS, Hurley LS. Age, sex and reproductive status alter the severity of anorexia in zinc deficient rats. Physiol Behav. 1986 Oct;38(4):485-93. PMID: 3469681
674: Leure-Dupree AE. Vascularization of the rat cornea after prolonged zinc deficiency. Anat Rec. 1986 Sep;216(1):27-32. PMID: 2429589
675: Li ET, O'Dell BL. Effect of zinc status on the binding of prostaglandins to ovarian membranes and intact platelets of pregnant rats. J Nutr. 1986 Aug;116(8):1448-55. PMID: 3463679
676: Lee JS, Fong LY. Decreased glutathione transferase activities in zinc-deficient rats. Carcinogenesis. 1986 Jul;7(7):1111-3. PMID: 3719905
677: Schrager TF, Busby WF Jr, Goldman ME, Newberne PM. Enhancement of methylbenzylnitrosamine-induced esophageal carcinogenesis in zinc-deficient rats: effects on incorporation of [3H]thymidine into DNA of esophageal epithelium and liver. Carcinogenesis. 1986 Jul;7(7):1121-6. PMID: 3719907
678: Rothman RJ, Leure-duPree AE, Fosmire GJ. Zinc deficiency affects the composition of the rat adrenal gland. Proc Soc Exp Biol Med. 1986 Jul;182(3):350-7. PMID: 3714717
679: Krieger I, Alpern BE, Cunnane SC. Transient neonatal zinc deficiency. Am J Clin Nutr. 1986 Jun;43(6):955-8. PMID: 3717070
680: Wada L, King JC. Effect of low zinc intakes on basal metabolic rate, thyroid hormones and protein utilization in adult men. J Nutr. 1986 Jun;116(6):1045-53. PMID: 3723200
681: Bray TM, Kubow S, Bettger WJ. Effect of dietary zinc on endogenous free radical production in rat lung microsomes. J Nutr. 1986 Jun;116(6):1054-60. PMID: 3014092
682: Record IR, Dreosti IE, Tulsi RS, Manuel SJ. Maternal metabolism and teratogenesis in zinc-deficient rats. Teratology. 1986 Jun;33(3):311-7. PMID: 3738824
683: Gupta RP, Verma PC, Gupta RK. Experimental zinc deficiency in guinea-pigs: biochemical changes. Br J Nutr. 1986 May;55(3):613-20. PMID: 3676179
684: Jhangiani S, Prince L, Holmes R, Agarwal N. Clinical zinc deficiency during long-term total enteral nutrition. J Am Geriatr Soc. 1986 May;34(5):385-8. PMID: 3082961
685: Fraker PJ, Gershwin ME, Good RA, Prasad A. Interrelationships between zinc and immune function. Fed Proc. 1986 Apr;45(5):1474-9. PMID: 3485544
686: Perez-Jimenez F, Bockman DE, Singh M. Pancreatic acinar cell function and morphology in rats fed zinc-deficient and marginal zinc-deficient diets. Gastroenterology. 1986 Apr;90(4):946-57. PMID: 2419200
687: Park JH, Grandjean CJ, Antonson DL, Vanderhoof JA. Effects of isolated zinc deficiency on the composition of skeletal muscle, liver and bone during growth in rats. J Nutr. 1986 Apr;116(4):610-7. PMID: 3958807
688: Tyrala EE. Zinc and copper balances in preterm infants. Pediatrics. 1986 Apr;77(4):513-7. PMID: 3960619
689: Garfinkel D. Is aging inevitable? The intracellular zinc deficiency hypothesis of aging. Med Hypotheses. 1986 Feb;19(2):117-37. Review. PMID: 3517602
690: Kuramoto Y, Igarashi Y, Kato S, Tagami H. Acquired zinc deficiency in two breast-fed mature infants. Acta Derm Venereol. 1986;66(4):359-61. PMID: 2430414
691: Barch DH, Iannaccone PM. Role of zinc deficiency in carcinogenesis. Adv Exp Med Biol. 1986;206:517-27. PMID: 3591537
692: Gallant KR, Cherian MG. Influence of maternal mineral deficiency on the hepatic metallothionein and zinc in newborn rats. Biochem Cell Biol. 1986 Jan;64(1):8-12. PMID: 3964467
693: Southon S, Gee JM, Johnson IT. Hexose absorption from jejunal loops in situ in zinc-deficient and Zn-supplemented rats. Br J Nutr. 1986 Jan;55(1):193-200. PMID: 3663574
694: Fong LY, Lui CP, NG WL, Newberne PM. The effect of N-nitrosodimethylamine and N-nitroso-N-benzylmethylamine on [3H]thymidine incorporation into the DNA of target and non-target tissues in the zinc-deficient rat. Cancer Lett. 1986 Jan;30(1):61-71. PMID: 3943081
695: Evans GW. Zinc and its deficiency diseases. Clin Physiol Biochem. 1986;4(1):94-8. Review. PMID: 3514057
696: Dura Trave T, Puig Abuli M, Monreal I, Villa Elizaga I. Plasmatic zinc concentrations during pregnancy in zinc-deficient rats in relation to neonatal outcome. Gynecol Obstet Invest. 1986;22(3):134-9. PMID: 3781344
697: Vannucchi H, Kutnink MD, Sauberlich M, Howerde E. Interaction among niacin, vitamin B6 and zinc in rats receiving ethanol. Int J Vitam Nutr Res. 1986;56(4):355-62. PMID: 3804611
698: Cunnane SC, Ainley CC, Keeling PW, Thompson RP, Crawford MA. Diminished phospholipid incorporation of essential fatty acids in peripheral blood leucocytes from patients with Crohn's disease: correlation with zinc depletion. J Am Coll Nutr. 1986;5(5):451-8. PMID: 3097102
699: Reeves PG, O'Dell BL. Effects of dietary zinc deprivation on the activity of angiotensin-converting enzyme in serum of rats and guinea pigs. J Nutr. 1986 Jan;116(1):128-34. PMID: 3003288
700: Waalkes MP. Effect of dietary zinc deficiency on the accumulation of cadmium and metallothionein in selected tissues of the rat. J Toxicol Environ Health. 1986;18(2):301-13. PMID: 3712492
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Zinc: 1000 Citations |
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701: Petit TL, LeBoutillier JC. Zinc deficiency in the postnatal rat: implications for lead toxicity. Neurotoxicology. 1986 Spring;7(1):237-46. PMID: 3714124
702: Perez-Jimenez F, Singh M, Bockman DE, Hahn HK. Interaction between marginal zinc deficiency and chronic alcoholism: pancreatic structure and function in rats in vitro. Pancreas. 1986;1(3):254-63. PMID: 2437569
703: Halas ES, Hunt CD, Eberhardt MJ. Learning and memory disabilities in young adult rats from mildly zinc deficient dams. Physiol Behav. 1986;37(3):451-8. PMID: 3749304
704: Styrud J, Dahlstrom VE, Eriksson UJ. Induction of skeletal malformations in the offspring of rats fed a zinc deficient diet. Ups J Med Sci. 1986;91(1):29-36. PMID: 3716021
705: Golub MS, Gershwin ME, Hurley LS, Hendrickx AG, Saito WY. Studies of marginal zinc deprivation in rhesus monkeys: infant behavior. Am J Clin Nutr. 1985 Dec;42(6):1229-39. PMID: 4072958
706: Zarling EJ, Mobarhan S, Donahue PE. Does zinc deficiency affect intestinal protein content or disaccharidase activity? J Lab Clin Med. 1985 Dec;106(6):708-11. PMID: 3934298
707: Park JH, Grandjean CJ, Antonson DL, Vanderhoof JA. Effects of short-term isolated zinc deficiency on intestinal growth and activities of several brush border enzymes in weaning rats. Pediatr Res. 1985 Dec;19(12):1333-6. PMID: 4080454
708: Record IR, Tulsi RS, Dreosti IE, Fraser FJ. Cellular necrosis in zinc-deficient rat embryos. Teratology. 1985 Dec;32(3):397-405. PMID: 4082071
709: Chen XC, Yin TA, He JS, Ma QY, Han ZM, Li LX. Low levels of zinc in hair and blood, pica, anorexia, and poor growth in Chinese preschool children. Am J Clin Nutr. 1985 Oct;42(4):694-700. PMID: 3863480
710: Sanecki RK, Corbin JE, Forbes RM. Extracutaneous histologic changes accompanying zinc deficiency in pups. Am J Vet Res. 1985 Oct;46(10):2120-3. PMID: 4062016
711: Wasik F, Baran E, Andrzejak R, Waniewska I, Sierawska M. [Zinc content of leukocytes and serum in psoriasis patients] Hautarzt. 1985 Oct;36(10):573-6. German. PMID: 4066318
712: Prasad AS. Clinical and biochemical manifestation zinc deficiency in human subjects. J Pharmacol. 1985 Oct-Dec;16(4):344-52. Review. PMID: 2419703
713: Gupta RP, Verma PC, Gupta RK. Experimental zinc deficiency in guinea-pigs: clinical signs and some haematological studies. Br J Nutr. 1985 Sep;54(2):421-8. PMID: 4063328
714: Keppen LD, Pysher T, Rennert OM. Zinc deficiency acts as a co-teratogen with alcohol in fetal alcohol syndrome. Pediatr Res. 1985 Sep;19(9):944-7. PMID: 4047764
715: Haynes DC, Gershwin ME, Golub MS, Cheung AT, Hurley LS, Hendrickx AG. Studies of marginal zinc deprivation in rhesus monkeys: VI. Influence on the immunohematology of infants in the first year. Am J Clin Nutr. 1985 Aug;42(2):252-62. PMID: 4025197
716: Prasad AS. Clinical, endocrinological and biochemical effects of zinc deficiency. Clin Endocrinol Metab. 1985 Aug;14(3):567-89. Review. PMID: 3905080
717: Daeschner CW 3rd, Carpentieri U, Goldman AS, Haggard ME. Zinc deficiency and blood lymphocyte function with sickle cell disease. Scand J Haematol. 1985 Aug;35(2):186-90. PMID: 3876597
718: Senapati A, Thompson RP. Zinc deficiency and the prolonged accumulation of zinc in wounds. Br J Surg. 1985 Jul;72(7):583-4. PMID: 4016546
719: Moran JR, Lyerly A. The effects of severe zinc deficiency on intestinal amino acid losses in the rat. Life Sci. 1985 Jul 1;36(26):2515-21. PMID: 4010465
720: Chisolm JC, Handorf CR. Zinc, cadmium, metallothionein, and progesterone: do they participate in the etiology of pregnancy induced hypertension? Med Hypotheses. 1985 Jul;17(3):231-42. Review. PMID: 3900651
721: Simmer K, Punchard NA, Murphy G, Thompson RP. Prostaglandin production and zinc depletion in human pregnancy. Pediatr Res. 1985 Jul;19(7):697-700. PMID: 4022677
722: Kruis W, Rindfleisch GE, Weinzierl M. Zinc deficiency as a problem in patients with Crohn's disease and fistula formation. Hepatogastroenterology. 1985 Jun;32(3):133-4. PMID: 4018707
723: Burke JP, Fenton MR. Effect of a zinc-deficient diet on lipid peroxidation in liver and tumor subcellular membranes. Proc Soc Exp Biol Med. 1985 Jun;179(2):187-91. PMID: 3991604
724: Record IR, Dreosti IE, Tulsi RS. In vitro development of zinc-deficient and replete rat embryos. Aust J Exp Biol Med Sci. 1985 Feb;63 ( Pt 1):65-71. PMID: 4015550
725: Schoelmerich J, Becher MS, Hoppe-Seyler P, Matern S, Haeussinger D, Loehle E, Koettgen E, Gerok W. Zinc and vitamin A deficiency in patients with Crohn's disease is correlated with activity but not with localization or extent of the disease. Hepatogastroenterology. 1985 Feb;32(1):34-8. PMID: 3988225
726: Wallwork JC, Duerre JA. Effect of zinc deficiency on methionine metabolism, methylation reactions and protein synthesis in isolated perfused rat liver. J Nutr. 1985 Feb;115(2):252-62. PMID: 3968590
727: Sato F, Watanabe T, Hoshi E, Endo A. Teratogenic effect of maternal zinc deficiency and its co-teratogenic effect with cadmium. Teratology. 1985 Feb;31(1):13-8. PMID: 3983855
728: Rogers JM, Keen CL, Hurley LS. Zinc deficiency in pregnant Long-Evans hooded rats: teratogenicity and tissue trace elements. Teratology. 1985 Feb;31(1):89-100. PMID: 3983863
729: Simmer K, Thompson RP. Zinc in the fetus and newborn. Acta Paediatr Scand Suppl. 1985;319:158-63. PMID: 3868917
730: Villa Elizaga I, da Cunha Ferreira RM. Zinc, pregnancy and parturition. Acta Paediatr Scand Suppl. 1985;319:150-7. PMID: 3868916
731: Prasad AS. Clinical manifestations of zinc deficiency. Annu Rev Nutr. 1985;5:341-63. Review. PMID: 3896271
732: Masters DG, Chapman RE, Vaughan JD. Effects of zinc deficiency on the wool growth, skin and wool follicles of pre-ruminant lambs. Aust J Biol Sci. 1985;38(4):355-64. PMID: 3834887
733: Murphy JF, Gray OP, Rendall JR, Hann S. Zinc deficiency: a problem with preterm breast milk. Early Hum Dev. 1985 Jan;10(3-4):303-7. PMID: 3987580
734: Prasad AS. Clinical and biochemical manifestations of zinc deficiency in human subjects. J Am Coll Nutr. 1985;4(1):65-72. Review. PMID: 2580877
735: Tapazoglou E, Prasad AS, Hill G, Brewer GJ, Kaplan J. Decreased natural killer cell activity in patients with zinc deficiency with sickle cell disease. J Lab Clin Med. 1985 Jan;105(1):19-22. PMID: 3968462
736: McClain CJ, Kasarskis EJ Jr, Allen JJ. Functional consequences of zinc deficiency. Prog Food Nutr Sci. 1985;9(1-2):185-226. Review. PMID: 3911268
737: Hallmans G, Lasek J. The effect of topical zinc absorption from wounds on growth and the wound healing process in zinc-deficient rats. Scand J Plast Reconstr Surg. 1985;19(2):119-25. PMID: 4070979
738: Prasad AS. Clinical, endocrinologic, and biochemical effects of zinc deficiency. Spec Top Endocrinol Metab. 1985;7:45-76. Review. PMID: 3914098
739: Leek JC, Vogler JB, Gershwin ME, Golub MS, Hurley LS, Hendrickx AG. Studies of marginal zinc deprivation in rhesus monkeys. V. Fetal and infant skeletal effects. Am J Clin Nutr. 1984 Dec;40(6):1203-12. PMID: 6507342
740: Golub MS, Gershwin ME, Hurley LS, Saito WY, Hendrickx AG. Studies of marginal zinc deprivation in rhesus monkeys. IV. Growth of infants in the first year. Am J Clin Nutr. 1984 Dec;40(6):1192-202. PMID: 6507341
741: Mountokalakis T, Dourakis S, Karatzas N, Maravelias C, Koutselinis A. Zinc deficiency in mild hypertensive patients treated with diuretics. J Hypertens Suppl. 1984 Dec;2(3):S571-2. PMID: 6152785
742: McClain CJ, Gavaler JS, Van Thiel DH. Hypogonadism in the zinc-deficient rat: localization of the functional abnormalities. J Lab Clin Med. 1984 Dec;104(6):1007-15. PMID: 6438259
743: Held DD, Hoekstra WG. The effects of zinc deficiency on turnover of cadmium-metallothionein in rat liver. J Nutr. 1984 Dec;114(12):2274-82. PMID: 6502271
744: Cunnane SC, Horrobin DF, Manku MS. Essential fatty acids in tissue phospholipids and triglycerides of the zinc-deficient rat. Proc Soc Exp Biol Med. 1984 Dec;177(3):441-6. PMID: 6440147
745: Chanmugam P, Wheeler C, Hwang DH. The effect of zinc deficiency on prostaglandin synthesis in rat testes. J Nutr. 1984 Nov;114(11):2066-72. PMID: 6593439
746: de Amorim CS, Collares EF, Rossi MA, Zucoloto S, de Souza NM. [Morphological study of the small intestine in rats with experimental zinc deficiency] Arq Gastroenterol. 1984 Oct-Dec;20(4):170-4. Portuguese. PMID: 6743049
747: Prasad AS. Discovery and importance of zinc in human nutrition. Fed Proc. 1984 Oct;43(13):2829-34. Review. PMID: 6383875
748: Das I, Burch RE, Hahn HK. Effects of zinc deficiency on ethanol metabolism and alcohol and aldehyde dehydrogenase activities. J Lab Clin Med. 1984 Oct;104(4):610-7. PMID: 6384394
749: DePasquale-Jardieu P, Fraker PJ. Interference in the development of a secondary immune response in mice by zinc deprivation: persistence of effects. J Nutr. 1984 Oct;114(10):1762-9. PMID: 6481473
750: Dvergsten CL, Fosmire GJ, Ollerich DA, Sandstead HH. Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. II. Impaired maturation of Purkinje cells. Brain Res. 1984 Sep;318(1):11-20. PMID: 6488049
751: Ghishan FK. Transport of electrolytes, water, and glucose in zinc deficiency. J Pediatr Gastroenterol Nutr. 1984 Sep;3(4):608-12. PMID: 6090631
752: Oner G, Bhaumick B, Bala RM. Effect of zinc deficiency on serum somatomedin levels and skeletal growth in young rats. Endocrinology. 1984 May;114(5):1860-3. PMID: 6714170
753: Kramer TR. Reevaluation of zinc deficiency on concanavalin-A-induced rat spleen lymphocyte proliferation. J Nutr. 1984 May;114(5):953-63. PMID: 6726465
754: Ng WL, Fong LY, Newberne PM. Forestomach squamous papillomas in the rat: effect of dietary zinc deficiency on induction. Cancer Lett. 1984 Apr;22(3):329-32. PMID: 6713373
755: Kumar SP, Anday EK. Edema, hypoproteinemia, and zinc deficiency in low-birth-weight infants. Pediatrics. 1984 Mar;73(3):327-9. PMID: 6701056
756: Essatara MB, Levine AS, Morley JE, McClain CJ. Zinc deficiency and anorexia in rats: normal feeding patterns and stress induced feeding. Physiol Behav. 1984 Mar;32(3):469-74. PMID: 6589654
757: Essatara MB, McClain CJ, Levine AS, Morley JE. Zinc deficiency and anorexia in rats: the effect of central administration of norepinephrine, muscimol and bromerogocryptine. Physiol Behav. 1984 Mar;32(3):479-82. PMID: 6589655
758: Golub MS, Gershwin ME, Hurley LS, Baly DL, Hendrickx AG. Studies of marginal zinc deprivation in rhesus monkeys. I. Influence on pregnant dams. Am J Clin Nutr. 1984 Feb;39(2):265-80. PMID: 6695828
759: Fong LY, Lee JS, Chan WC, Newberne PM. Zinc deficiency and the development of esophageal and forestomach tumors in Sprague-Dawley rats fed precursors of N-nitroso-N-benzylmethylamine. J Natl Cancer Inst. 1984 Feb;72(2):419-25. PMID: 6582327
760: Dura Trave T, Puig Abuli M, da Cunha Ferreira RM, Villa Elizaga I. Effect of zinc nutrition on parturition and postpartum in the rat. Gynecol Obstet Invest. 1984;18(5):275-80. PMID: 6526343
761: Fong LY, Ng WL, Newberne PM. N-nitrosodimethylamine-induced forestomach tumours in male Sprague-Dawley rats fed a zinc-deficient diet. IARC Sci Publ. 1984;(57):543-6. PMID: 6533046
762: Prasad AS. Zinc deficiency in sickle cell disease. Prog Clin Biol Res. 1984;165:49-58. PMID: 6504920
763: Wenk GL, Stemmer KL. Suboptimal dietary zinc intake increases aluminum accumulation into the rat brain. Brain Res. 1983 Dec 12;288(1-2):393-5. PMID: 6661634
764: Beach RS, Gershwin ME, Hurley LS. Persistent immunological consequences of gestation zinc deprivation. Am J Clin Nutr. 1983 Oct;38(4):579-90. PMID: 6624700
765: Allen JI, Perri RT, McClain CJ, Kay NE. Alterations in human natural killer cell activity and monocyte cytotoxicity induced by zinc deficiency. J Lab Clin Med. 1983 Oct;102(4):577-89. PMID: 6604771
766: Wallwork JC, Milne DB, Sims RL, Sandstead HH. Severe zinc deficiency: effects on the distribution of nine elements (potassium, phosphorus, sodium, magnesium, calcium, iron, zinc, copper and manganese) in regions of the rat brain. J Nutr. 1983 Oct;113(10):1895-905. PMID: 6619970
767: Greeley S, Sandstead HH. Oxidation of alanine and beta-hydroxybutyrate in late gestation by zinc-restricted rats. J Nutr. 1983 Sep;113(9):1803-10. PMID: 6411876
768: Dvergsten CL, Fosmire GJ, Ollerich DA, Sandstead HH. Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. I. Impaired acquisition of granule cells. Brain Res. 1983 Jul 25;271(2):217-26. PMID: 6616175
769: Bronson DM, Barsky R, Barsky S. Acrodermatitis enteropathica. J Am Acad Dermatol. 1983 Jul;9(1):140-4. PMID: 6886096
770: Carpentieri U, Smith L, Daeschner CW 3rd, Haggard ME. Neutrophils and zinc in infection-prone children with sickle cell disease. Pediatrics. 1983 Jul;72(1):88-92. PMID: 6866596
771: Arlette JP. Zinc and the skin. Pediatr Clin North Am. 1983 Jun;30(3):583-96. Review. PMID: 6348687
772: Roth HP, Kirchgessner M. [Effect of zinc deficiency on 3',5'-cyclic-AMP content and parameters of energy metabolism in the rat] Z Ernahrungswiss. 1983 Jun;22(2):116-23. German. PMID: 6308919
773: Cunnane SC, Majid E, Senior J, Mills CF. Uteroplacental dysfunction and prostaglandin metabolism in zinc deficient pregnant rats. Life Sci. 1983 May 23;32(21):2471-8. PMID: 6406778
774: Reeves PG, O'Dell BL. The effect of zinc deficiency on glucose metabolism in meal-fed rats. Br J Nutr. 1983 May;49(3):441-52. PMID: 6860624
775: Masters DG, Moir RJ. Effect of zinc deficiency on the pregnant ewe and developing foetus. Br J Nutr. 1983 May;49(3):365-72. PMID: 6860622
776: Masters DG, Keen CL, Lonnerdal B, Hurley LS. Zinc deficiency teratogenicity: the protective role of maternal tissue catabolism. J Nutr. 1983 Apr;113(4):905-12. PMID: 6834156
777: Gebhard RL, Karouani R, Prigge WF, McClain CJ. The effect of severe zinc deficiency on activity of intestinal disaccharidases and 3-hydroxy-3-methylglutaryl coenzyme A reductase in the rat. J Nutr. 1983 Apr;113(4):855-9. PMID: 6403680
778: Gordon PR, Browning JD, O'Dell BL. Platelet arachidonate metabolism and platelet function in zinc-deficient rats. J Nutr. 1983 Apr;113(4):766-72. PMID: 6403678
779: Halas ES, Eberhardt MJ, Diers MA, Sandstead HH. Learning and memory impairment in adult rats due to severe zinc deficiency during lactation. Physiol Behav. 1983 Mar;30(3):371-81. PMID: 6867134
780: Golub MS, Gershwin ME, Vijayan VK. Passive avoidance performance of mice fed marginally or severely zinc deficient diets during post-embryonic brain development. Physiol Behav. 1983 Mar;30(3):409-13. PMID: 6867137
781: Ballester OF, Prasad AS. Anergy, zinc deficiency, and decreased nucleoside phosphorylase activity in patients with sickle cell anemia. Ann Intern Med. 1983 Feb;98(2):180-2. PMID: 6401957
782: McMurray DN, Yetley EA. Response to Mycobacterium bovis BCG vaccination in protein- and zinc-deficient guinea pigs. Infect Immun. 1983 Feb;39(2):755-61. PMID: 6339390
783: McMurray DN, Carlomagno MA, Cumberland PA. Respiratory infection with attenuated Mycobacterium tuberculosis H37Ra in malnourished guinea pigs. Infect Immun. 1983 Feb;39(2):793-9. PMID: 6403460
784: Ayala S, Brenner RR. Essential fatty acid status in zinc deficiency. Effect on lipid and fatty acid composition, desaturation activity and structure of microsomal membranes of rat liver and testes. Acta Physiol Lat Am. 1983;33(3):193-204. PMID: 6673505
785: Zhavoronkov AA. [Zinc-deficient states in man] Arkh Patol. 1983;45(9):77-80. Review. Russian. PMID: 6360097
786: Aggett PJ. Acrodermatitis enteropathica. J Inherit Metab Dis. 1983;6 Suppl 1:39-43. PMID: 6413773
787: Miller SI, Del Villano BC, Flynn A, Krumhansl M. Interaction of alcohol and zinc in fetal dysmorphogenesis. Pharmacol Biochem Behav. 1983;18 Suppl 1:311-5. PMID: 6634846
788: Cavdar AO, Arcasoy A, Cin S, Babacan E, Gozdasoglu S. Geophagia in Turkey: iron and zinc deficiency, iron and zinc absorption studies and response to treatment with zinc in geophagia cases. Prog Clin Biol Res. 1983;129:71-97. PMID: 6657708
789: Cavdar AO, Babacan E, Asik S, Arcasoy A, Ertem U, Himmetoglu O, Baycu T, Akar N. Zinc levels of serum, plasma, erythrocytes and hair in Turkish women with anencephalic babies. Prog Clin Biol Res. 1983;129:99-106. PMID: 6657709
790: Prasad AS. Zinc deficiency in human subjects. Prog Clin Biol Res. 1983;129:1-33. Review. PMID: 6361778
791: Prasad AS, Cossack ZT. Zinc in sickle cell disease. Trans Assoc Am Physicians. 1983;96:246-51. PMID: 6388101
792: Mahajan SK, Prasad AS, Rabbani P, Briggs WA, McDonald FD. Zinc deficiency: a reversible complication of uremia. Am J Clin Nutr. 1982 Dec;36(6):1177-83. PMID: 6890761
793: Beach RS, Gershwin ME, Hurley LS. Nutritional factors and autoimmunity. III. Zinc deprivation versus restricted food intake in MRL/1 mice--the distinction between interacting dietary influences. J Immunol. 1982 Dec;129(6):2686-92. PMID: 6982939
794: Schmidt H, Riemann JF, Grosse KP. [Clinical aspects, diagnosis and therapy of acrodermatitis enteropathica] Leber Magen Darm. 1982 Nov;12(6):239-44. German. PMID: 6306369
795: Reyes AJ, Leary WP, Lockett CJ, Alcocer L. Diuretics and zinc. S Afr Med J. 1982 Sep 4;62(11):373-5. PMID: 7112305
796: Sanecki RK, Corbin JE, Forbes RM. Tissue changes in dogs fed a zinc-deficient ration. Am J Vet Res. 1982 Sep;43(9):1642-6. PMID: 7149412
797: Mahajan SK, Abbasi AA, Prasad AS, Rabbani P, Briggs WA, McDonald FD. Effect of oral zinc therapy on gonadal function in hemodialysis patients. A double-blind study. Ann Intern Med. 1982 Sep;97(3):357-61. PMID: 7051913
798: Massaro TF, Mohs M, Fosmire G. Effects of moderate zinc deficiency on cognitive performance in young adult rats. Physiol Behav. 1982 Jul;29(1):117-21. PMID: 7122717
799: Meydani SN, Dupont J. Effect of zinc deficiency on prostaglandin synthesis in different organs of the rat. J Nutr. 1982 Jun;112(6):1098-104. PMID: 7045297
800: Beach RS, Gershwin ME, Hurley LS. Reversibility of development retardation following murine fetal zinc deprivation. J Nutr. 1982 Jun;112(6):1169-81. PMID: 7086545
801: Fraker PJ, Caruso R, Kierszenbaum F. Alteration of the immune and nutritional status of mice by synergy between zinc deficiency and infection with Trypanosoma cruzi. J Nutr. 1982 Jun;112(6):1224-9. PMID: 6806454
802: Briggs WA, Pedersen MM, Mahajan SK, Sillix DH, Prasad AS, McDonald FD. Lymphocyte and granulocyte function in zinc-treated and zinc-deficient hemodialysis patients. Kidney Int. 1982 Jun;21(6):827-32. PMID: 7132052
803: Cunnane SC. Foetal mortality in moderately zinc-deficient rats is strictly related to the process of parturition: effect of maternal essential fatty acid supplementation. Br J Nutr. 1982 May;47(3):495-504. PMID: 7082621
804: Gabrial GN, Schrager TF, Newberne PM. Zinc deficiency, alcohol, and retinoid: association with esophageal cancer in rats. J Natl Cancer Inst. 1982 May;68(5):785-9. PMID: 6951089
805: Gordon EF, Bond JT, Gordon RC, Denny MR. Zinc deficiency and behavior: a development perspective. Physiol Behav. 1982 May;28(5):893-7. PMID: 7100289
806: Rothbaum RJ, Maur PR, Farrell MK. Serum alkaline phosphatase and zinc undernutrition in infants with chronic diarrhea. Am J Clin Nutr. 1982 Mar;35(3):595-8. PMID: 6801964
807: Odutuga AA. Effects of low-zinc status and essential fatty acid deficiency on growth and lipid composition of rat brain. Clin Exp Pharmacol Physiol. 1982 Mar-Apr;9(2):213-21. PMID: 7127918
808: Moran DM, Russo J Jr, Bell LV. Zinc deficiency dermatitis accompanying parenteral nutrition supplemented with trace elements. Clin Pharm. 1982 Mar-Apr;1(2):169-76. PMID: 6821033
809: Halas ES, Wallwork JC, Sandstead HH. Mild zinc deficiency and undernutrition during the prenatal and postnatal periods in rats: effects on weight, food consumption, and brain catecholamine concentrations. J Nutr. 1982 Mar;112(3):542-51. PMID: 7062148
810: Hsu JM, Rubenstein B. Effect of zinc deficiency on histidine metabolism in rats. J Nutr. 1982 Mar;112(3):461-7. PMID: 6121018
811: Clejan S, Castro-Magana M, Collipp PJ, Jonas E, Maddaiah VT. Effects of zinc deficiency and castration on fatty acid composition and desaturation in rats. Lipids. 1982 Mar;17(3):129-35. PMID: 7087688
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825: Ruth RE, Goldsmith SK. Interaction between zinc deprivation and acute ethanol intoxication during pregnancy in rats. J Nutr. 1981 Nov;111(11):2034-8. PMID: 7197711
826: Cheek DB, Smith RM, Spargo RM, Francis N. Zinc, copper and environmental factors in the aboriginal peoples of the North West. Aust N Z J Med. 1981 Oct;11(5):508-12. PMID: 6948543
827: Cerklewski FL. Effect of suboptimal zinc nutrition during gestation and lactation on rat molar tooth composition and dental caries. J Nutr. 1981 Oct;111(10):1780-3. PMID: 7288500
828: Bates J, McClain CJ. The effect of severe zinc deficiency on serum levels of albumin, transferrin, and prealbumin in man. Am J Clin Nutr. 1981 Sep;34(9):1655-60. PMID: 6792896
829: Jakinovich W Jr, Osborn DW. Zinc nutrition and salt preference in rats. Am J Physiol. 1981 Sep;241(3):R233-9. PMID: 7282969
830: Siegler RL, Eggert JV, Udomkesmalee E. Diagnostic indices of zinc deficiency in children with renal diseases. Ann Clin Lab Sci. 1981 Sep-Oct;11(5):428-33. PMID: 7332311
831: Hambidge KM. Zinc deficiency in man: its origins and effects. Philos Trans R Soc Lond B Biol Sci. 1981 Aug 14;294(1071):129-44. PMID: 6118891
832: Allen JI, Kay NE, McClain CJ. Severe zinc deficiency in humans: association with a reversible T-lymphocyte dysfunction. Ann Intern Med. 1981 Aug;95(2):154-7. PMID: 6789737
833: Fitzsimons RB, Soltan MH. Congenital skin defects and zinc deficiency - a possible relationship. Eur J Obstet Gynecol Reprod Biol. 1981 Aug;12(2):79-84. PMID: 7198590
834: Herlong HF, Russell RM, Maddrey WC. Vitamin A and zinc therapy in primary biliary cirrhosis. Hepatology. 1981 Jul-Aug;1(4):348-51. PMID: 7286911
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836: Denko CW, Petricevic M, Whitehouse MW. Inflammation in relation to dietary intake of zinc and copper. Int J Tissue React. 1981 Jun;3(2):73-6. PMID: 7327617
837: Mills BJ, Lindeman RD, Lang CA. Effect of zinc deficiency on blood glutathione levels. J Nutr. 1981 Jun;111(6):1098-102. PMID: 7241230
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839: Cheek DB, Spargo RM, Holt AB. Evidence for zinc deficiency in aboriginal settlements in Northwestern Australia. Med J Aust. 1981 May 2;1(2 Suppl):4-5. PMID: 7254081
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845: Reeves PG, O'Dell BL. Short-term zinc deficiency in the rat and self-section of dietary protein level. J Nutr. 1981 Feb;111(2):375-83. PMID: 7463176
846: Kreavich ME, Meyer J, Waterhouse JP. Increased numbers of mast cells in the hyperplastic buccal mucosa of the zinc-deficient rat. J Oral Pathol. 1981 Feb;10(1):22-31. PMID: 6782206
847: Reid GM. The pharmacological role of zinc: evidence from clinical studies on animals. Med Hypotheses. 1981 Feb;7(2):207-15. PMID: 7219245
848: Weismann K, Hagdrup HK. Hair changes due to zinc deficiency in a case of sucrose malabsorption. Acta Derm Venereol. 1981;61(5):444-7. PMID: 6172938
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850: Prasad AS. Zinc deficiency and effects of zinc supplementation on sickle cell anemia subjects. Prog Clin Biol Res. 1981;55:99-122. PMID: 7291206
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852: Good RA, West A, Fernandes G. Nutritional modulation of immune responses. Fed Proc. 1980 Nov;39(13):3098-104. PMID: 6968692
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854: Gordon PR, O'Dell BL. Rat platelet aggregation impaired by short-term zinc deficiency. J Nutr. 1980 Oct;110(10):2125-9. PMID: 6775060
855: Abbasi AA, Prasad AS, Rabbani P, DuMouchelle E. Experimental zinc deficiency in man. Effect on testicular function. J Lab Clin Med. 1980 Sep;96(3):544-50. PMID: 6772723
856: Morley JE, Gordon J, Hershman JM. Zinc deficiency, chronic starvation, and hypothalamic-pituitary-thyroid function. Am J Clin Nutr. 1980 Aug;33(8):1767-70. PMID: 7405879
857: Greeley S, Fosmire GJ, Sandstead HH. Nitrogen retention during late gestation in the rat in response to marginal zinc intake. Am J Physiol. 1980 Aug;239(2):E113-8. PMID: 7406040
858: Hsieh HS, Navia JM. Zinc deficiency and bone formation in guinea pig alveolar implants. J Nutr. 1980 Aug;110(8):1581-8. PMID: 7400848
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861: Fang MM, Lei KY, Kilgore LT. Effects of zinc deficiency on dental caries in rats. J Nutr. 1980 May;110(5):1032-6. PMID: 7373428
862: Chandra RK, Au B. Single nutrient deficiency and cell-mediated immune responses. I. Zinc. Am J Clin Nutr. 1980 Apr;33(4):736-8. PMID: 6987859
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864: Swenerton H, Hurley LS. Zinc deficiency in rhesus and bonnet monkeys, including effects on reproduction. J Nutr. 1980 Mar;110(3):575-83. PMID: 6767006
865: McClain C, Soutor C, Zieve L. Zinc deficiency: a complication of Crohn's disease. Gastroenterology. 1980 Feb;78(2):272-9. PMID: 7350050
866: Beach RS, Gershwin ME, Hurley LS. Growth and development in postnatally zinc-deprived mice. J Nutr. 1980 Feb;110(2):201-11. PMID: 7354391
867: Weismann K, Hoyer H, Christensen E. Acquired zinc deficiency in alcoholic liver cirrhosis: report of two cases. Acta Derm Venereol. 1980;60(5):447-9. PMID: 6162323
868: Bonifazi E, Rigillo N, De Simone B, Meneghini CL. Acquired dermatitis due to zinc deficiency in a premature infant. Acta Derm Venereol. 1980;60(5):449-51. PMID: 6162324
869: Sullivan JF, Jetton MM, Hahn HK, Burch RE. Enhanced lipid peroxidation in liver microsomes of zinc-deficient rats. Am J Clin Nutr. 1980 Jan;33(1):51-6. PMID: 7355780
870: Mutch PB, Hurley LS. Mammary gland function and development: effect of zinc deficiency in rat. Am J Physiol. 1980 Jan;238(1):E26-31. PMID: 7356013
871: Lamand M, Lab C, Tressol JC. Comparison of the efficiency of zinc injected as metal or oxide for zinc deficiency treatment in sheep. Ann Rech Vet. 1980;11(2):147-9. PMID: 7192961
872: Elmes ME, Jones JG. Ultrastructural studies on Paneth cell apoptosis in zinc deficient rats. Cell Tissue Res. 1980;208(1):57-63. PMID: 7388931
873: Elmes ME, Jones JG. Ultrastructural changes in the small intestine of zinc deficient rats. J Pathol. 1980 Jan;130(1):37-43. PMID: 7381626
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878: Solomons NW. Trace minerals in paediatric gastroenterology: zinc and copper. Arq Gastroenterol. 1979 Oct-Dec;16(4):209-16. Review. PMID: 121692
879: Hesse GW. Chronic zinc deficiency alters neuronal function of hippocampal mossy fibers. Science. 1979 Sep 7;205(4410):1005-7. PMID: 224456
880: Abou-Mourad NN, Farah FS, Steel D. Dermopathic changes in hypozincemia. Arch Dermatol. 1979 Aug;115(8):956-8. PMID: 111624
881: Chen SY. Focal epithelial hyperplasia in rabbit oral mucosa. J Oral Pathol. 1979 Aug;8(4):213-23. PMID: 115979
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885: Bakan R. The role of zinc in anorexia nervosa: etiology and treatment. Med Hypotheses. 1979 Jul;5(7):731-6. PMID: 514114
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887: Catalanotto FA. Alterations of short-term tastant-containing fluid intake in zinc deficient adult rats. J Nutr. 1979 Jun;109(6):1079-85. PMID: 448447
888: Root AW, Duckett G, Sweetland M, Reiter EO. Effects of zinc deficiency upon pituitary function in sexually mature and immature male rats. J Nutr. 1979 Jun;109(6):958-64. PMID: 376793
889: Jackson AJ, Schumacher HJ. The teratogenic activity of a thalidomide analogus EM12 in rats on a low-zinc diet. Teratology. 1979 Jun;19(3):341-4. PMID: 473085
890: Brazin SA, Johnson WT, Abramson LJ. The acrodermatitis enteropathica-like syndrome. Arch Dermatol. 1979 May;115(5):597-9. PMID: 109049
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896: Mathur A, Wallenius K, Abdulla M. Influence of zinc on onset and progression of oral carcinogenesis in rats. Acta Odontol Scand. 1979;37(5):277-84. PMID: 118633
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898: Hoitsma HF, Cuesta MA, Starink TM, Uttendorfsky-van der Putten HJ, van der Veen EA. Zinc deficiency syndrome versus glucagonoma syndrome. Arch Chir Neerl. 1979;31(3):131-40. PMID: 534435
899: Weismann K. Intravenous zinc sulfate therapy in zinc-depleted patients. Dermatologica. 1979;159(2):171-5. PMID: 478053
900: Abbasi AA, Prasad AS, Rabbani PR. Experimental zinc deficiency in man: effect on spermatogenesis. Trans Assoc Am Physicians. 1979;92:292-302. PMID: 549254
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902: Atkin-Thor E, Goddard BW, O'Nion J, Stephen RL, Kolff WJ. Hypogeusia and zinc depletion in chronic dialysis patients. Am J Clin Nutr. 1978 Oct;31(10):1948-51. PMID: 707353
903: Prasad AS, Rabbani P, Abbasii A, Bowersox E, Fox MR. Experimental zinc deficiency in humans. Ann Intern Med. 1978 Oct;89(4):483-90. PMID: 697227
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911: Sandstead HH, Strobel DA, Logan GM Jr, Marks EO, Jacob RA. Zinc deficiency in pregnant rhesus monkeys: effects on behavior of infants. Am J Clin Nutr. 1978 May;31(5):844-9. PMID: 417617
912: Chesters JK, Will M. Effect of age, weight and adequacy of zinc intake on the balance between alkaline ribonuclease and ribonuclease inhibitor in various tissues of the rat. Br J Nutr. 1978 Mar;39(2):375-82. PMID: 415757
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925: Belanger LF, Casas-Cordero M, Urist MR. The effects of zinc deprivation on the host response to intramuscular bone matrix implants in the rat. Clin Orthop. 1977 Jun;(125):208-13. PMID: 880769
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